Alexei Drummond deleted bibliography/ComputationalEvolution.bib  over 8 years ago

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%% This BibTeX bibliography file was created using BibDesk.  %% http://bibdesk.sourceforge.net/  %% Created for alexei at 2015-09-03 17:03:39 +0200   %% Saved with string encoding Unicode (UTF-8)   @string{aac = {Antimicrobial Agents and Chemotherapy}}  @string{acc = {Antiviral Chemisty and Chemotherapy}}  @string{aids = {AIDS}}  @string{aidshr = {Journal of Acquired Immunodeficiency Syndrone and Human Retrovirology}}  @string{aim = {Annals of Internal Medicine}}  @string{aje = {American Journal of Epidemiology}}  @string{arhr = {AIDS Research and Human Retroviruses}}  @string{as = {The American Statistician}}  @string{bm = {Biometrics}}  @string{cdc = {Centers for Disease Control}}  @string{cii = {Clinical Immunology and Immunopathology}}  @string{cs = {Clinical Science (London)}}  @string{drugs = {Drugs}}  @string{eid = {Emerging Infectious Diseases}}  @string{embo = {EMBO J}}  @string{ian = {International Antiviral News}}  @string{il = {Immunology Letters}}  @string{jac = {Journal of Antimicrob Chemother}}  @string{jama = {Journal of the American Medical Association}}  @string{jasa = {Journal of the American Statistical Association}}  @string{jbc = {Journal of Biological Chemistry}}  @string{jbiochem = {Journal of Biological Chemistry}}  @string{jci = {Journal of Clinical Investigations}}  @string{jem = {Journal of Experimental Medicine}}  @string{jid = {Journal of Infectious Disease}}  @string{jscs = {Journal of Statistical Computation and Simulation}}  @string{jv = {Journal of Virology}}  @string{lanc = {Lancet}}  @string{lda = {Lifetime Data Analysis}}  @string{mmwr = {Morbidity and Mortality Weekly Report}}  @string{na = {Nature}}  @string{nejm = {New England Journal of Medicine}}  @string{ni = {Nature Immunology}}  @string{nm = {Nature Medicine}}  @string{pnas = {Proceedings of the National Acadamy of Science USA}}  @string{sc = {Science}}  @string{sm = {Statistics in Medicine}}  @string{ss = {Statistical Science}}  @article{LangleyFitch1974,  Author = {Langley, C H and Fitch, W M},  Date-Added = {2015-09-03 14:56:34 +0000},  Date-Modified = {2015-09-03 15:03:36 +0000},  Journal = {J Mol Evol},  Journal-Full = {Journal of molecular evolution},  Mesh = {Animals; Biological Evolution; Blood Proteins; Cytochrome c Group; DNA; Deoxyribonucleotides; Diploidy; Fibrin; Genes; Genetics, Population; Hemoglobins; Mathematics; Models, Biological; Mutation; Probability; Protein Biosynthesis; RNA; Ribonucleotides; Species Specificity; Time Factors; Transcription, Genetic; Vertebrates},  Number = {3},  Pages = {161-77},  Pmid = {4368400},  Pst = {ppublish},  Title = {An examination of the constancy of the rate of molecular evolution},  Volume = {3},  Year = {1974}}  @article{Kimura:1989eu,  Abstract = {The main tenet of the neutral theory is that the great majority of evolutionary changes at the molecular level are caused not by Darwinian selection but by random fixation of selectively neutral (or very nearly neutral) alleles through random sampling drift under continued mutation pressure. The theory also asserts that the majority of protein and DNA polymorphisms are selectively neutral, and that they are maintained in the species by mutational input balanced by random extinction rather than by "balancing selection." The neutral theory is based on simple assumptions. This enabled us to develop mathematical theories (using the diffusion equation method) that can treat these phenomena in quantitative terms and that permit theory to be tested against actual observations. Although the neutral theory has been severely criticized by the neo-Darwinian establishment, supporting evidence has accumulated over the last 20 years. In particular, the recent burst of DNA sequence data helped to strengthen the theory a great deal. I believe that the neutral theory triggered reexamination of the traditional "synthetic theory of evolution." In this paper, I review the present status of the neutral theory, including discussions of such topics as "molecular evolutionary clock," very high evolutionary rates observed in RNA viruses, a deviant coding system found in Mycoplasm together with the concept of mutation-driven neutral evolution, and the origin of life. I also present a worldview based on the conception of what I call "survival of the luckiest."},  Author = {Kimura, M},  Date-Added = {2015-09-03 14:01:57 +0000},  Date-Modified = {2015-09-03 14:01:57 +0000},  Journal = {Genome},  Journal-Full = {Genome / National Research Council Canada = G{\'e}nome / Conseil national de recherches Canada},  Mesh = {Animals; Biological Evolution; DNA; History, 19th Century; History, 20th Century; Humans; Molecular Biology; Mutation; Selection, Genetic},  Number = {1},  Pages = {24-31},  Pmid = {2687096},  Pst = {ppublish},  Title = {The neutral theory of molecular evolution and the world view of the neutralists},  Volume = {31},  Year = {1989}}  @article{Gojobori:1990yg,  Abstract = {Evolution of viral genes is characterized by enormously high speed compared with that of nuclear genes of eukaryotic organisms. In this paper, the evolutionary rates and patterns of base substitutions are examined for retroviral oncogenes, human immunodeficiency viruses (HIV), hepatitis B viruses (HBV), and influenza A viruses. Our results show that the evolutionary process of these viral genes can readily be explained by the neutral theory of molecular evolution. In particular, the neutral theory is supported by our observation that synonymous substitutions always much predominate over nonsynonymous substitutions, even though the substitution rate varies considerably among the viruses. Furthermore, the exact correspondence between the high rates of evolutionary base substitutions and the high rates of production of mutants in RNA viruses fits very nicely to the prediction of the theory. The linear relationship between substitution numbers and time was examined to evaluate the clock-like property of viral evolution. The clock appears to be quite accurate in the influenza A viruses in man.},  Author = {Gojobori, T and Moriyama, E N and Kimura, M},  Date-Added = {2015-09-03 14:01:50 +0000},  Date-Modified = {2015-09-03 14:01:50 +0000},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Biological Evolution; DNA, Viral; Genes, Viral; HIV; Hepatitis B virus; Humans; Models, Genetic; Phylogeny; Retroviridae; Viruses},  Month = {Dec},  Number = {24},  Pages = {10015-8},  Pmc = {PMC55305},  Pmid = {2263602},  Pst = {ppublish},  Title = {Molecular clock of viral evolution, and the neutral theory},  Volume = {87},  Year = {1990}}  @article{Kimura1987,  Abstract = {From the standpoint of the neutral theory of molecular evolution, it is expected that a universally valid and exact molecular evolutionary clock would exist if, for a given molecule, the mutation rate for neutral alleles per year were exactly equal among all organisms at all times. Any deviation from the equality of neutral mutation rate per year makes the molecular clock less exact. Such deviation may be due to two causes: one is the change of the mutation rate per year (such as due to change of generation span), and the other is the alteration of the selective constraint of each molecule (due to change of internal molecular environment). A statistical method was developed to investigate the equality of evolutionary rates among lineages. This was used to analyze protein data to demonstrate that these two causes are actually at work in molecular evolution. It was emphasized that departures from exact clockwise progression of molecular evolution by no means invalidates the neutral theory. It was pointed out that experimental studies should be done to settle the issue of whether the mutation rate for nucleotide change is more constant per year or per generation among organisms whose generation spans are very different.},  Author = {Kimura, M},  Date-Added = {2015-09-03 14:01:43 +0000},  Date-Modified = {2015-09-03 14:02:23 +0000},  Journal = {J Mol Evol},  Journal-Full = {Journal of molecular evolution},  Mesh = {Alleles; Animals; Biological Evolution; Genes; Genetics, Population; Hemoglobins; Humans; Models, Genetic; Mutation; Species Specificity},  Number = {1-2},  Pages = {24-33},  Pmid = {3125335},  Pst = {ppublish},  Title = {Molecular evolutionary clock and the neutral theory},  Volume = {26},  Year = {1987}}  @book{Yang:2006yu,  Address = {Oxford},  Annote = {LDR 01691cam 22004217a 4500  001 14755574  005 20070620113543.0  008 070302s2006 enka b 001 0 eng d  906 $a7$bcbc$ccopycat$d2$encip$f20$gy-gencatlg  925 0 $aacquire$b2 shelf copies$xpolicy default  955 $apv21 2007-03-02 z-processor to ASCD$ijx85 2007-03-06$ejx85 2007-03-06 to BCCD$asf32 2007-04-02 copy 2 added  010 $a 2007271492  015 $aGBA685429$2bnb  016 7 $a101292306$2DNLM  016 7 $a013572476$2Uk  020 $a0198566999  020 $a9780198566991  020 $a0198567022 (pbk.)  020 $a9780198567028 (pbk.)  035 $a(OCoLC)ocm72868007  040 $aNLM$cNLM$dUKM$dBAKER$dBWKUK$dYDXCP$dIXA$dAGL$dDLC  042 $aukblsr$anlmcopyc$alccopycat  050 00 $aQH371.3.M37$bY36 2006  060 10 $aQU 475$bY21c 2006  060 00 $a2006 M-551  070 0 $aQH371.3.M37$bY36 2006  082 04 $a572.838015118$222  100 1 $aYang, Ziheng.  245 10 $aComputational molecular evolution /$cZiheng Yang.  260 $aOxford :$bOxford University Press,$c2006.  300 $axvi, 357 p. :$bill. ;$c24 cm.  440 0 $aOxford series in ecology and evolution  504 $aIncludes bibliographical references (p. [319]-352) and index.  650 0 $aMolecular evolution$xMathematical models.  650 0 $aMolecular evolution$xData processing.  856 41 $3Table of contents only$uhttp://www.loc.gov/catdir/toc/fy0711/2007271492.html  856 42 $3Contributor biographical information$uhttp://www.loc.gov/catdir/enhancements/fy0726/2007271492-b.html  856 42 $3Publisher description$uhttp://www.loc.gov/catdir/enhancements/fy0726/2007271492-d.html  },  Author = {Yang, Ziheng},  Call-Number = {QH371.3.M37},  Date-Added = {2015-08-11 13:32:21 +0000},  Date-Modified = {2015-08-11 13:32:21 +0000},  Dewey-Call-Number = {572.838015118},  Genre = {Molecular evolution},  Isbn = {0198566999},  Library-Id = {2007271492},  Publisher = {Oxford University Press},  Title = {Computational molecular evolution},  Url = {http://www.loc.gov/catdir/toc/fy0711/2007271492.html},  Year = {2006},  Bdsk-Url-1 = {http://www.loc.gov/catdir/toc/fy0711/2007271492.html}}  @article{tavare1986some,  Author = {Tavar{\'e}, Simon},  Date-Added = {2015-07-02 04:41:35 +0000},  Date-Modified = {2015-07-02 04:41:35 +0000},  Journal = {Lectures on mathematics in the life sciences},  Pages = {57--86},  Title = {Some probabilistic and statistical problems in the analysis of DNA sequences},  Volume = {17},  Year = {1986}}  @article{Rodriguez:1990bh,  Abstract = {DNA sequence evolution through nucleotide substitution may be assimilated to a stationary Markov process. The fundamental equations of the general model, with 12 independent substitution parameters, are used to obtain a formula which corrects the effect of multiple and parallel substitutions on the measure of evolutionary divergence between two homologous sequences. We show that only reversible models, with six independent parameters, allow the calculation of the substitution rates. Simulation experiments on DNA sequence evolution through nucleotide substitution call into question the effectiveness of the general model (and of any other more detailed description); nevertheless, the general model results are slightly superior to any of its particular cases.},  Author = {Rodr{\'\i}guez, F and Oliver, J L and Mar{\'\i}n, A and Medina, J R},  Date-Added = {2015-07-02 04:39:08 +0000},  Date-Modified = {2015-07-02 04:39:08 +0000},  Journal = {J Theor Biol},  Journal-Full = {Journal of theoretical biology},  Mesh = {Animals; Base Sequence; Biological Evolution; Computer Simulation; DNA; Markov Chains; Models, Biological},  Month = {Feb},  Number = {4},  Pages = {485-501},  Pmid = {2338834},  Pst = {ppublish},  Title = {The general stochastic model of nucleotide substitution},  Volume = {142},  Year = {1990}}  @article{Benner:2014kq,  Abstract = {MOTIVATION: The construction of statistics for summarizing posterior samples returned by a Bayesian phylogenetic study has so far been hindered by the poor geometric insights available into the space of phylogenetic trees, and ad hoc methods such as the derivation of a consensus tree makeup for the ill-definition of the usual concepts of posterior mean, while bootstrap methods mitigate the absence of a sound concept of variance. Yielding satisfactory results with sufficiently concentrated posterior distributions, such methods fall short of providing a faithful summary of posterior distributions if the data do not offer compelling evidence for a single topology.  RESULTS: Building upon previous work of Billera et al., summary statistics such as sample mean, median and variance are defined as the geometric median, Fr{\'e}chet mean and variance, respectively. Their computation is enabled by recently published works, and embeds an algorithm for computing shortest paths in the space of trees. Studying the phylogeny of a set of plants, where several tree topologies occur in the posterior sample, the posterior mean balances correctly the contributions from the different topologies, where a consensus tree would be biased. Comparisons of the posterior mean, median and consensus trees with the ground truth using simulated data also reveals the benefits of a sound averaging method when reconstructing phylogenetic trees.  AVAILABILITY AND IMPLEMENTATION: We provide two independent implementations of the algorithm for computing Fr{\'e}chet means, geometric medians and variances in the space of phylogenetic trees. TFBayes: https://github.com/pbenner/tfbayes, TrAP: https://github.com/bacak/TrAP.  CONTACT: [email protected].},  Author = {Benner, Philipp and Ba{\v c}{\'a}k, Miroslav and Bourguignon, Pierre-Yves},  Date-Added = {2014-09-23 22:59:22 +0000},  Date-Modified = {2014-09-23 22:59:22 +0000},  Doi = {10.1093/bioinformatics/btu461},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Month = {Sep},  Number = {17},  Pages = {i534-i540},  Pmc = {PMC4147914},  Pmid = {25161244},  Pst = {ppublish},  Title = {Point estimates in phylogenetic reconstructions},  Volume = {30},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/btu461}}  @article{owen2011fast,  Author = {Owen, Megan and Provan, J Scott},  Date-Added = {2014-08-03 21:16:48 +0000},  Date-Modified = {2014-08-03 21:16:48 +0000},  Journal = {IEEE/ACM Transactions on Computational Biology and Bioinformatics (TCBB)},  Number = {1},  Pages = {2--13},  Publisher = {IEEE Computer Society Press},  Title = {A fast algorithm for computing geodesic distances in tree space},  Volume = {8},  Year = {2011}}  @article{lunn2009bugs,  Author = {Lunn, David J. and Spiegelhalter, David and Thomas, Andrew and Best, Nicky},  Date-Added = {2014-08-03 02:38:33 +0000},  Date-Modified = {2014-12-04 01:10:13 +0000},  Journal = {Statistics in medicine},  Number = {25},  Pages = {3049--3067},  Publisher = {Wiley Online Library},  Title = {The BUGS project: Evolution, critique and future directions},  Volume = {28},  Year = {2009}}  @article{lunn2000winbugs,  Author = {Lunn, David J. and Thomas, Andrew and Best, Nicky and Spiegelhalter, David},  Date-Added = {2014-08-03 02:37:03 +0000},  Date-Modified = {2014-12-04 01:09:56 +0000},  Journal = {Statistics and computing},  Number = {4},  Pages = {325--337},  Publisher = {Springer},  Title = {WinBUGS -- a Bayesian modelling framework: concepts, structure, and extensibility},  Volume = {10},  Year = {2000}}  @misc{stan-software:2014,  Author = {{Stan Development Team}},  Date-Added = {2014-08-03 02:34:49 +0000},  Date-Modified = {2014-08-03 02:34:49 +0000},  Title = {Stan: A C++ Library for Probability and Sampling, Version 2.4},  Url = {http://mc-stan.org/},  Year = {2014},  Bdsk-Url-1 = {http://mc-stan.org/}}  @article{HoffmanGelman2013,  Author = {Hoffman, Matthew D. and Gelman, Andrew},  Date-Added = {2014-08-03 02:33:43 +0000},  Date-Modified = {2014-08-03 02:34:00 +0000},  Journal = {Journal of Machine Learning Research},  Number = {Apr},  Pages = {1593--1623},  Title = {The No-{U}-Turn Sampler: Adaptively Setting Path Lengths in {H}amiltonian {M}onte {C}arlo},  Volume = {15},  Year = {2014}}  @article{Jones2011,  Author = {Jones, Graham},  Journal = {Journal of mathematical biology},  Number = {1},  Pages = {33--56},  Publisher = {Springer},  Title = {Calculations for multi-type age-dependent binary branching processes},  Volume = {63},  Year = {2011}}  @article{hurvich1989regression,  Author = {Hurvich, Clifford M and Tsai, Chih-Ling},  Date-Added = {2014-07-20 23:42:06 +0000},  Date-Modified = {2014-07-20 23:42:06 +0000},  Journal = {Biometrika},  Number = {2},  Pages = {297--307},  Publisher = {Biometrika Trust},  Title = {Regression and time series model selection in small samples},  Volume = {76},  Year = {1989}}  @article{akaike1974new,  Author = {Akaike, Hirotugu},  Date-Added = {2014-07-20 23:16:58 +0000},  Date-Modified = {2014-07-20 23:16:58 +0000},  Journal = {Automatic Control, IEEE Transactions on},  Number = {6},  Pages = {716--723},  Publisher = {Ieee},  Title = {A new look at the statistical model identification},  Volume = {19},  Year = {1974}}  @article{akaike1976information,  Author = {Akaike, H},  Date-Added = {2014-07-20 23:15:18 +0000},  Date-Modified = {2014-07-20 23:15:18 +0000},  Journal = {Math Sci},  Number = {153},  Pages = {5--9},  Title = {An information criterion (AIC)},  Volume = {14},  Year = {1976}}  @inproceedings{akaike1973information,  Author = {Akaike, H},  Booktitle = {International symposium on information theory, Second edition},  Date-Added = {2014-07-20 23:09:44 +0000},  Date-Modified = {2014-07-20 23:15:17 +0000},  Editor = {Petrov, B. N. and Cs{\'a}ski, F},  Pages = {267--281},  Publisher = {Akademiai Kiado, Budapest, Hungary},  Title = {Information theory and an extension of the maximum likelihood principle.},  Volume = {2},  Year = {1973}}  @article{Baele:2013kq,  Abstract = {Recent implementations of path sampling (PS) and stepping-stone sampling (SS) have been shown to outperform the harmonic mean estimator (HME) and a posterior simulation-based analog of Akaike's information criterion through Markov chain Monte Carlo (AICM), in bayesian model selection of demographic and molecular clock models. Almost simultaneously, a bayesian model averaging approach was developed that avoids conditioning on a single model but averages over a set of relaxed clock models. This approach returns estimates of the posterior probability of each clock model through which one can estimate the Bayes factor in favor of the maximum a posteriori (MAP) clock model; however, this Bayes factor estimate may suffer when the posterior probability of the MAP model approaches 1. Here, we compare these two recent developments with the HME, stabilized/smoothed HME (sHME), and AICM, using both synthetic and empirical data. Our comparison shows reassuringly that MAP identification and its Bayes factor provide similar performance to PS and SS and that these approaches considerably outperform HME, sHME, and AICM in selecting the correct underlying clock model. We also illustrate the importance of using proper priors on a large set of empirical data sets.},  Author = {Baele, Guy and Li, Wai Lok Sibon and Drummond, Alexei J and Suchard, Marc A and Lemey, Philippe},  Date-Added = {2014-07-20 22:54:44 +0000},  Date-Modified = {2014-07-20 22:54:44 +0000},  Doi = {10.1093/molbev/mss243},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Animals; Bayes Theorem; Computer Simulation; Evolution, Molecular; Humans; Models, Genetic; Phylogeny},  Month = {Feb},  Number = {2},  Pages = {239-43},  Pmc = {PMC3548314},  Pmid = {23090976},  Pst = {ppublish},  Title = {Accurate model selection of relaxed molecular clocks in bayesian phylogenetics},  Volume = {30},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/mss243}}  @electronic{rambaut2014tracer,  Author = {Rambaut, A and Drummond, A. J.},  Date-Added = {2014-07-20 06:01:25 +0000},  Date-Modified = {2014-07-20 06:05:10 +0000},  Title = {Tracer v1.6},  Url = {http://tree.bio.ed.ac.uk/software/tracer/},  Year = {2014},  Bdsk-Url-1 = {http://tree.bio.ed.ac.uk/software/tracer/}}  @article{steel2010expected,  Author = {Steel, Mike and Mooers, Arne},  Date-Added = {2014-07-18 00:18:53 +0000},  Date-Modified = {2014-07-18 00:18:53 +0000},  Journal = {Applied Mathematics Letters},  Number = {11},  Pages = {1315--1319},  Publisher = {Elsevier},  Title = {The expected length of pendant and interior edges of a Yule tree},  Volume = {23},  Year = {2010}}  @article{Edgar2004throughput,  Abstract = {We describe MUSCLE, a new computer program for creating multiple alignments of protein sequences. Elements of the algorithm include fast distance estimation using kmer counting, progressive alignment using a new profile function we call the log-expectation score, and refinement using tree-dependent restricted partitioning. The speed and accuracy of MUSCLE are compared with T-Coffee, MAFFT and CLUSTALW on four test sets of reference alignments: BAliBASE, SABmark, SMART and a new benchmark, PREFAB. MUSCLE achieves the highest, or joint highest, rank in accuracy on each of these sets. Without refinement, MUSCLE achieves average accuracy statistically indistinguishable from T-Coffee and MAFFT, and is the fastest of the tested methods for large numbers of sequences, aligning 5000 sequences of average length 350 in 7 min on a current desktop computer. The MUSCLE program, source code and PREFAB test data are freely available at http://www.drive5. com/muscle.},  Author = {Edgar, Robert C},  Date-Added = {2014-07-17 20:15:34 +0000},  Date-Modified = {2014-07-17 20:15:52 +0000},  Doi = {10.1093/nar/gkh340},  Journal = {Nucleic Acids Res},  Journal-Full = {Nucleic acids research},  Mesh = {Algorithms; Amino Acid Motifs; Amino Acid Sequence; Internet; Molecular Sequence Data; Reproducibility of Results; Sequence Alignment; Sequence Analysis, Protein; Software; Time Factors},  Number = {5},  Pages = {1792-7},  Pmc = {PMC390337},  Pmid = {15034147},  Pst = {epublish},  Title = {MUSCLE: multiple sequence alignment with high accuracy and high throughput},  Volume = {32},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/nar/gkh340}}  @article{Edgar2004complexity,  Abstract = {BACKGROUND: In a previous paper, we introduced MUSCLE, a new program for creating multiple alignments of protein sequences, giving a brief summary of the algorithm and showing MUSCLE to achieve the highest scores reported to date on four alignment accuracy benchmarks. Here we present a more complete discussion of the algorithm, describing several previously unpublished techniques that improve biological accuracy and / or computational complexity. We introduce a new option, MUSCLE-fast, designed for high-throughput applications. We also describe a new protocol for evaluating objective functions that align two profiles.  RESULTS: We compare the speed and accuracy of MUSCLE with CLUSTALW, Progressive POA and the MAFFT script FFTNS1, the fastest previously published program known to the author. Accuracy is measured using four benchmarks: BAliBASE, PREFAB, SABmark and SMART. We test three variants that offer highest accuracy (MUSCLE with default settings), highest speed (MUSCLE-fast), and a carefully chosen compromise between the two (MUSCLE-prog). We find MUSCLE-fast to be the fastest algorithm on all test sets, achieving average alignment accuracy similar to CLUSTALW in times that are typically two to three orders of magnitude less. MUSCLE-fast is able to align 1,000 sequences of average length 282 in 21 seconds on a current desktop computer.  CONCLUSIONS: MUSCLE offers a range of options that provide improved speed and / or alignment accuracy compared with currently available programs. MUSCLE is freely available at http://www.drive5.com/muscle.},  Author = {Edgar, Robert C},  Date-Added = {2014-07-17 20:15:34 +0000},  Date-Modified = {2014-07-17 20:16:05 +0000},  Doi = {10.1186/1471-2105-5-113},  Journal = {BMC Bioinformatics},  Journal-Full = {BMC bioinformatics},  Mesh = {Cluster Analysis; Computational Biology; Phylogeny; Sequence Alignment; Software; Software Design; Time Factors},  Month = {Aug},  Pages = {113},  Pmc = {PMC517706},  Pmid = {15318951},  Pst = {epublish},  Title = {MUSCLE: a multiple sequence alignment method with reduced time and space complexity},  Volume = {5},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2105-5-113}}  @article{Katoh2013,  Abstract = {We report a major update of the MAFFT multiple sequence alignment program. This version has several new features, including options for adding unaligned sequences into an existing alignment, adjustment of direction in nucleotide alignment, constrained alignment and parallel processing, which were implemented after the previous major update. This report shows actual examples to explain how these features work, alone and in combination. Some examples incorrectly aligned by MAFFT are also shown to clarify its limitations. We discuss how to avoid misalignments, and our ongoing efforts to overcome such limitations.},  Author = {Katoh, Kazutaka and Standley, Daron M},  Date-Added = {2014-07-17 20:15:34 +0000},  Date-Modified = {2014-07-17 20:16:35 +0000},  Doi = {10.1093/molbev/mst010},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Algorithms; Amino Acid Sequence; Base Sequence; DNA, Fungal; DNA, Ribosomal; DNA, Ribosomal Spacer; Fungi; Humans; Models, Genetic; Molecular Sequence Data; Phylogeny; Protein Structure, Tertiary; Quality Improvement; RNA, Bacterial; Ribonucleases; Ribosome Subunits, Small, Bacterial; Sequence Alignment; Software},  Month = {Apr},  Number = {4},  Pages = {772-80},  Pmc = {PMC3603318},  Pmid = {23329690},  Pst = {ppublish},  Title = {MAFFT multiple sequence alignment software version 7: improvements in performance and usability},  Volume = {30},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/mst010}}  @article{Katoh2014,  Abstract = {This chapter outlines several methods implemented in the MAFFT package. MAFFT is a popular multiple sequence alignment (MSA) program with various options for the progressive method, the iterative refinement method and other methods. We first outline basic usage of MAFFT and then describe recent practical extensions, such as dot plot and adjustment of direction in DNA alignment. We also refer to MUSCLE, another high-performance MSA program.},  Author = {Katoh, Kazutaka and Standley, Daron M},  Date-Added = {2014-07-17 20:15:34 +0000},  Date-Modified = {2014-07-17 20:16:40 +0000},  Doi = {10.1007/978-1-62703-646-7_8},  Journal = {Methods Mol Biol},  Journal-Full = {Methods in molecular biology (Clifton, N.J.)},  Mesh = {Computational Biology; Computers; DNA; RNA; Sequence Alignment; Software},  Pages = {131-46},  Pmid = {24170399},  Pst = {ppublish},  Title = {MAFFT: iterative refinement and additional methods},  Volume = {1079},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1007/978-1-62703-646-7_8}}  @article{Katoh2002,  Abstract = {A multiple sequence alignment program, MAFFT, has been developed. The CPU time is drastically reduced as compared with existing methods. MAFFT includes two novel techniques. (i) Homo logous regions are rapidly identified by the fast Fourier transform (FFT), in which an amino acid sequence is converted to a sequence composed of volume and polarity values of each amino acid residue. (ii) We propose a simplified scoring system that performs well for reducing CPU time and increasing the accuracy of alignments even for sequences having large insertions or extensions as well as distantly related sequences of similar length. Two different heuristics, the progressive method (FFT-NS-2) and the iterative refinement method (FFT-NS-i), are implemented in MAFFT. The performances of FFT-NS-2 and FFT-NS-i were compared with other methods by computer simulations and benchmark tests; the CPU time of FFT-NS-2 is drastically reduced as compared with CLUSTALW with comparable accuracy. FFT-NS-i is over 100 times faster than T-COFFEE, when the number of input sequences exceeds 60, without sacrificing the accuracy.},  Author = {Katoh, Kazutaka and Misawa, Kazuharu and Kuma, Kei-ichi and Miyata, Takashi},  Date-Added = {2014-07-17 20:15:34 +0000},  Date-Modified = {2014-07-17 20:16:46 +0000},  Journal = {Nucleic Acids Res},  Journal-Full = {Nucleic acids research},  Mesh = {Computer Simulation; DNA-Directed RNA Polymerases; RNA, Ribosomal; Reproducibility of Results; Sequence Alignment; Software; Spectroscopy, Fourier Transform Infrared},  Month = {Jul},  Number = {14},  Pages = {3059-66},  Pmc = {PMC135756},  Pmid = {12136088},  Pst = {ppublish},  Title = {MAFFT: a novel method for rapid multiple sequence alignment based on fast Fourier transform},  Volume = {30},  Year = {2002}}  @article{BrownYang2011,  Abstract = {BACKGROUND: Understanding causes of biological diversity may be greatly enhanced by knowledge of divergence times. Strict and relaxed clock models are used in Bayesian estimation of divergence times. We examined whether: i) strict clock models are generally more appropriate in shallow phylogenies where rate variation is expected to be low, ii) the likelihood ratio test of the clock (LRT) reliably informs which model is appropriate for dating divergence times. Strict and relaxed models were used to analyse sequences simulated under different levels of rate variation. Published shallow phylogenies (Black bass, Primate-sucking lice, Podarcis lizards, Gallotiinae lizards, and Caprinae mammals) were also analysed to determine natural levels of rate variation relative to the performance of the different models.  RESULTS: Strict clock analyses performed well on data simulated under the independent rates model when the standard deviation of log rate on branches, σ, was low (≤ 0.1), but were inappropriate when σ>0.1 (95% of rates fall within 0.0082-0.0121 subs/site/Ma when σ = 0.1, for a mean rate of 0.01). The independent rates relaxed clock model performed well at all levels of rate variation, although posterior intervals on times were significantly wider than for the strict clock. The strict clock is therefore superior when rate variation is low. The performance of a correlated rates relaxed clock model was similar to the strict clock. Increased numbers of independent loci led to slightly narrower posteriors under the relaxed clock while older root ages provided proportionately narrower posteriors. The LRT had low power for σ = 0.01-0.1, but high power for σ = 0.5-2.0. Posterior means of σ2 were useful for assessing rate variation in published datasets. Estimates of natural levels of rate variation ranged from 0.05-3.38 for different partitions. Differences in divergence times between relaxed and strict clock analyses were greater in two datasets with higher σ2 for one or more partitions, supporting the simulation results.  CONCLUSIONS: The strict clock can be superior for trees with shallow roots because of low levels of rate variation between branches. The LRT allows robust assessment of suitability of the clock model as does examination of posteriors on σ2.},  Author = {Brown, Richard P and Yang, Ziheng},  Date-Added = {2014-07-16 20:14:43 +0000},  Date-Modified = {2014-07-16 20:15:27 +0000},  Doi = {10.1186/1471-2148-11-271},  Journal = {BMC Evol Biol},  Journal-Full = {BMC evolutionary biology},  Mesh = {Animals; Bass; Bayes Theorem; Computer Simulation; Evolution, Molecular; Genetic Variation; Lizards; Models, Genetic; Mutation Rate; Phthiraptera; Phylogeny; Ruminants; Time Factors},  Pages = {271},  Pmc = {PMC3205074},  Pmid = {21943087},  Pst = {epublish},  Title = {Rate variation and estimation of divergence times using strict and relaxed clocks},  Volume = {11},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2148-11-271}}  @article{Heath2014fossilized,  Abstract = {Time-calibrated species phylogenies are critical for addressing a wide range of questions in evolutionary biology, such as those that elucidate historical biogeography or uncover patterns of coevolution and diversification. Because molecular sequence data are not informative on absolute time, external data-most commonly, fossil age estimates-are required to calibrate estimates of species divergence dates. For Bayesian divergence time methods, the common practice for calibration using fossil information involves placing arbitrarily chosen parametric distributions on internal nodes, often disregarding most of the information in the fossil record. We introduce the "fossilized birth-death" (FBD) process-a model for calibrating divergence time estimates in a Bayesian framework, explicitly acknowledging that extant species and fossils are part of the same macroevolutionary process. Under this model, absolute node age estimates are calibrated by a single diversification model and arbitrary calibration densities are not necessary. Moreover, the FBD model allows for inclusion of all available fossils. We performed analyses of simulated data and show that node age estimation under the FBD model results in robust and accurate estimates of species divergence times with realistic measures of statistical uncertainty, overcoming major limitations of standard divergence time estimation methods. We used this model to estimate the speciation times for a dataset composed of all living bears, indicating that the genus Ursus diversified in the Late Miocene to Middle Pliocene.},  Author = {Heath, Tracy A and Huelsenbeck, John P and Stadler, Tanja},  Date-Added = {2014-07-16 09:46:43 +0000},  Date-Modified = {2014-07-16 09:47:03 +0000},  Doi = {10.1073/pnas.1319091111},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Keywords = {Bayesian divergence time estimation; MCMC; phylogenetics; relaxed clock; time tree},  Month = {Jul},  Pmid = {25009181},  Pst = {aheadofprint},  Title = {The fossilized birth-death process for coherent calibration of divergence-time estimates},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.1319091111}}  @article{Romero2014,  Author = {Romero-Severson, Ethan and Skar, Helena and Bulla, Ingo and Albert, Jan and Leitner, Thomas},  Journal = {Molecular biology and evolution},  Pages = {msu179},  Publisher = {SMBE},  Title = {Timing and order of transmission events is not directly reflected in a pathogen phylogeny},  Year = {2014}}  @article{leitner1999phylogenetics,  Author = {Leitner, Thomas and Fitch, W},  Journal = {The evolution of HIV. Johns Hopkins University Press, Baltimore, Md},  Pages = {315--345},  Title = {The phylogenetics of known transmission histories},  Year = {1999}}  @article{didelot2014bayesian,  Author = {Didelot, Xavier and Gardy, Jennifer and Colijn, Caroline},  Journal = {Molecular biology and evolution},  Pages = {msu121},  Publisher = {SMBE},  Title = {Bayesian inference of infectious disease transmission from whole genome sequence data},  Year = {2014}}  @article{Wu2013,  Abstract = {Probabilistic inference of a phylogenetic tree from molecular sequence data is predicated on a substitution model describing the relative rates of change between character states along the tree for each site in the multiple sequence alignment. Commonly, one assumes that the substitution model is homogeneous across sites within large partitions of the alignment, assigns these partitions a priori, and then fixes their underlying substitution model to the best-fitting model from a hierarchy of named models. Here, we introduce an automatic model selection and model averaging approach within a Bayesian framework that simultaneously estimates the number of partitions, the assignment of sites to partitions, the substitution model for each partition, and the uncertainty in these selections. This new approach is implemented as an add-on to the BEAST 2 software platform. We find that this approach dramatically improves the fit of the nucleotide substitution model compared with existing approaches, and we show, using a number of example data sets, that as many as nine partitions are required to explain the heterogeneity in nucleotide substitution process across sites in a single gene analysis. In some instances, this improved modeling of the substitution process can have a measurable effect on downstream inference, including the estimated phylogeny, relative divergence times, and effective population size histories.},  Author = {Wu, Chieh-Hsi and Suchard, Marc A and Drummond, Alexei J},  Date-Added = {2014-07-13 12:55:21 +0000},  Date-Modified = {2014-07-13 12:55:40 +0000},  Doi = {10.1093/molbev/mss258},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Algorithms; Animals; Bayes Theorem; Cluster Analysis; Computer Simulation; Ebolavirus; Evolution, Molecular; Genome, Viral; Hepacivirus; Humans; Markov Chains; Models, Genetic; Monte Carlo Method; Phylogeny; Point Mutation; Respiratory Syncytial Viruses; Sequence Alignment; Software},  Month = {Mar},  Number = {3},  Pages = {669-88},  Pmc = {PMC3563969},  Pmid = {23233462},  Pst = {ppublish},  Title = {Bayesian selection of nucleotide substitution models and their site assignments},  Volume = {30},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/mss258}}  @article{Hohna:2011vn,  Abstract = {The birth-death process is widely used in phylogenetics to model speciation and extinction. Recent studies have shown that the inferred rates are sensitive to assumptions about the sampling probability of lineages. Here, we examine the effect of the method used to sample lineages. Whereas previous studies have assumed random sampling (RS), we consider two extreme cases of biased sampling: "diversified sampling" (DS), where tips are selected to maximize diversity and "cluster sampling (CS)," where sample diversity is minimized. DS appears to be standard practice, for example, in analyses of higher taxa, whereas CS may occur under special circumstances, for example, in studies of geographically defined floras or faunas. Using both simulations and analyses of empirical data, we show that inferred rates may be heavily biased if the sampling strategy is not modeled correctly. In particular, when a diversified sample is treated as if it were a random or complete sample, the extinction rate is severely underestimated, often close to 0. Such dramatic errors may lead to serious consequences, for example, if estimated rates are used in assessing the vulnerability of threatened species to extinction. Using Bayesian model testing across 18 empirical data sets, we show that DS is commonly a better fit to the data than complete, random, or cluster sampling (CS). Inappropriate modeling of the sampling method may at least partly explain anomalous results that have previously been attributed to variation over time in birth and death rates.},  Author = {H{\"o}hna, Sebastian and Stadler, Tanja and Ronquist, Fredrik and Britton, Tom},  Date-Added = {2014-07-13 12:29:55 +0000},  Date-Modified = {2014-07-13 12:29:55 +0000},  Doi = {10.1093/molbev/msr095},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Algorithms; Animals; Bayes Theorem; Birds; Computer Simulation; Extinction, Biological; Genetic Speciation; Models, Genetic; Phylogeny; Selection Bias},  Month = {Sep},  Number = {9},  Pages = {2577-89},  Pmid = {21482666},  Pst = {ppublish},  Title = {Inferring speciation and extinction rates under different sampling schemes},  Volume = {28},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msr095}}  @article{Mollentze:2014qy,  Abstract = {We describe a statistical framework for reconstructing the sequence of transmission events between observed cases of an endemic infectious disease using genetic, temporal and spatial information. Previous approaches to reconstructing transmission trees have assumed all infections in the study area originated from a single introduction and that a large fraction of cases were observed. There are as yet no approaches appropriate for endemic situations in which a disease is already well established in a host population and in which there may be multiple origins of infection, or that can enumerate unobserved infections missing from the sample. Our proposed framework addresses these shortcomings, enabling reconstruction of partially observed transmission trees and estimating the number of cases missing from the sample. Analyses of simulated datasets show the method to be accurate in identifying direct transmissions, while introductions and transmissions via one or more unsampled intermediate cases could be identified at high to moderate levels of case detection. When applied to partial genome sequences of rabies virus sampled from an endemic region of South Africa, our method reveals several distinct transmission cycles with little contact between them, and direct transmission over long distances suggesting significant anthropogenic influence in the movement of infected dogs.},  Author = {Mollentze, Nardus and Nel, Louis H and Townsend, Sunny and le Roux, Kevin and Hampson, Katie and Haydon, Daniel T and Soubeyrand, Samuel},  Date-Added = {2014-07-13 11:30:39 +0000},  Date-Modified = {2014-07-13 11:30:39 +0000},  Doi = {10.1098/rspb.2013.3251},  Journal = {Proc Biol Sci},  Journal-Full = {Proceedings. Biological sciences / The Royal Society},  Keywords = {endemic disease; rabies virus; spatial epidemiology; surveillance; transmission trees},  Month = {May},  Number = {1782},  Pages = {20133251},  Pmc = {PMC3973266},  Pmid = {24619442},  Pst = {epublish},  Title = {A Bayesian approach for inferring the dynamics of partially observed endemic infectious diseases from space-time-genetic data},  Volume = {281},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rspb.2013.3251}}  @article{Ford:2011bh,  Abstract = {Tuberculosis poses a global health emergency, which has been compounded by the emergence of drug-resistant Mycobacterium tuberculosis (Mtb) strains. We used whole-genome sequencing to compare the accumulation of mutations in Mtb isolated from cynomolgus macaques with active, latent or reactivated disease. We sequenced 33 Mtb isolates from nine macaques with an average genome coverage of 93% and an average read depth of 117×. Based on the distribution of SNPs observed, we calculated the mutation rates for these disease states. We found a similar mutation rate during latency as during active disease or in a logarithmically growing culture over the same period of time. The pattern of polymorphisms suggests that the mutational burden in vivo is because of oxidative DNA damage. We show that Mtb continues to acquire mutations during disease latency, which may explain why isoniazid monotherapy for latent tuberculosis is a risk factor for the emergence of isoniazid resistance.},  Author = {Ford, Christopher B and Lin, Philana Ling and Chase, Michael R and Shah, Rupal R and Iartchouk, Oleg and Galagan, James and Mohaideen, Nilofar and Ioerger, Thomas R and Sacchettini, James C and Lipsitch, Marc and Flynn, JoAnne L and Fortune, Sarah M},  Date-Added = {2014-07-12 10:57:23 +0000},  Date-Modified = {2014-07-12 10:57:23 +0000},  Doi = {10.1038/ng.811},  Journal = {Nat Genet},  Journal-Full = {Nature genetics},  Mesh = {Animals; Antitubercular Agents; Base Sequence; DNA, Bacterial; Disease Models, Animal; Drug Resistance, Bacterial; Genome, Bacterial; Humans; Isoniazid; Latent Tuberculosis; Macaca fascicularis; Models, Genetic; Mutation; Mycobacterium tuberculosis; Polymorphism, Single Nucleotide; Time Factors; Tuberculosis, Multidrug-Resistant},  Month = {May},  Number = {5},  Pages = {482-6},  Pmc = {PMC3101871},  Pmid = {21516081},  Pst = {ppublish},  Title = {Use of whole genome sequencing to estimate the mutation rate of Mycobacterium tuberculosis during latent infection},  Volume = {43},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/ng.811}}  @article{heled2013calibrated,  Author = {Heled, Joseph and Drummond, Alexei J},  Date-Added = {2014-07-12 09:18:44 +0000},  Date-Modified = {2014-07-12 09:18:44 +0000},  Journal = {arXiv preprint arXiv:1311.4921},  Title = {Calibrated birth-death phylogenetic time-tree priors for Bayesian inference},  Year = {2013}}  @article{Ronquist:2012fv,  Abstract = {Phylogenies are usually dated by calibrating interior nodes against the fossil record. This relies on indirect methods that, in the worst case, misrepresent the fossil information. Here, we contrast such node dating with an approach that includes fossils along with the extant taxa in a Bayesian total-evidence analysis. As a test case, we focus on the early radiation of the Hymenoptera, mostly documented by poorly preserved impression fossils that are difficult to place phylogenetically. Specifically, we compare node dating using nine calibration points derived from the fossil record with total-evidence dating based on 343 morphological characters scored for 45 fossil (4--20 complete) and 68 extant taxa. In both cases we use molecular data from seven markers (∼5 kb) for the extant taxa. Because it is difficult to model speciation, extinction, sampling, and fossil preservation realistically, we develop a simple uniform prior for clock trees with fossils, and we use relaxed clock models to accommodate rate variation across the tree. Despite considerable uncertainty in the placement of most fossils, we find that they contribute significantly to the estimation of divergence times in the total-evidence analysis. In particular, the posterior distributions on divergence times are less sensitive to prior assumptions and tend to be more precise than in node dating. The total-evidence analysis also shows that four of the seven Hymenoptera calibration points used in node dating are likely to be based on erroneous or doubtful assumptions about the fossil placement. With respect to the early radiation of Hymenoptera, our results suggest that the crown group dates back to the Carboniferous, ∼309 Ma (95% interval: 291--347 Ma), and diversified into major extant lineages much earlier than previously thought, well before the Triassic. [Bayesian inference; fossil dating; morphological evolution; relaxed clock; statistical phylogenetics.].},  Author = {Ronquist, Fredrik and Klopfstein, Seraina and Vilhelmsen, Lars and Schulmeister, Susanne and Murray, Debra L and Rasnitsyn, Alexandr P},  Date-Added = {2014-07-12 08:56:08 +0000},  Date-Modified = {2014-07-12 08:56:08 +0000},  Doi = {10.1093/sysbio/sys058},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Mesh = {Animals; Fossils; Genetic Speciation; Hymenoptera; Models, Genetic; Models, Statistical; Phylogeny; Statistics as Topic; Time Factors},  Month = {Dec},  Number = {6},  Pages = {973-99},  Pmc = {PMC3478566},  Pmid = {22723471},  Pst = {ppublish},  Title = {A total-evidence approach to dating with fossils, applied to the early radiation of the hymenoptera},  Volume = {61},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/sys058}}  @article{LeitnerAlbert1999,  Abstract = {Detailed knowledge about the rate and mode of the genetic variation is vital for understanding how HIV-1 induces disease and develops resistance as well as for studies on the molecular epidemiology and origin of the virus. To unveil the molecular clock of HIV-1 we analyzed a unique set of viruses from a known transmission history with separation times between samples of up to 25 years. The env V3 and p17gag regions of the genome were sequenced, and genetic distances were estimated by using the true tree and a nucleotide substitution model based on a general reversible Markov process with a gamma distribution to account for differences in substitution rates among sites. Linear regression analysis showed that separation times were significantly correlated with synonymous as well as nonsynonymous nucleotide distances in both V3 and p17, giving strong support for the existence of a molecular clock. The estimated rate of nucleotide substitution was 6.7 +/- 2.1 x 10(-3) substitutions/site per year in V3 and 2.7 +/- 0.5 x 10(-3) in p17. Importantly, the regression analyses showed that there was a significant genetic distance at zero divergence times. This pretransmission interval exists because the ramifications in the phylogenetic trees do not correspond to time of transmission, but rather to the coalescence time of the most recent common ancestor of the viruses carried by the transmitter and the recipient. Simulation experiments showed that neither the V3 nor the p17 clocks were overdispersed, which indicates that the introduction of nucleotide substitutions can be described adequately by a simple stochastic Poisson process.},  Author = {Leitner, T and Albert, J},  Date-Added = {2014-07-12 08:44:47 +0000},  Date-Modified = {2014-07-12 08:45:01 +0000},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Disease Transmission, Infectious; Evolution, Molecular; Gene Products, env; Gene Products, gag; Genetic Variation; HIV-1; Humans; Infectious Disease Transmission, Vertical; Models, Genetic; Molecular Sequence Data; Time Factors},  Month = {Sep},  Number = {19},  Pages = {10752-7},  Pmc = {PMC17955},  Pmid = {10485898},  Pst = {ppublish},  Title = {The molecular clock of HIV-1 unveiled through analysis of a known transmission history},  Volume = {96},  Year = {1999}}  @article{fearnhead2006exact,  Author = {Fearnhead, Paul and Sherlock, Chris},  Date-Added = {2014-07-07 10:23:45 +0000},  Date-Modified = {2014-07-07 10:23:45 +0000},  Journal = {Journal of the Royal Statistical Society: Series B (Statistical Methodology)},  Number = {5},  Pages = {767--784},  Publisher = {Wiley Online Library},  Title = {An exact Gibbs sampler for the Markov-modulated Poisson process},  Volume = {68},  Year = {2006}}  @article{Rodrigue2008,  Abstract = {MOTIVATION: Mapping character state changes over phylogenetic trees is central to the study of evolution. However, current probabilistic methods for generating such mappings are ill-suited to certain types of evolutionary models, in particular, the widely used models of codon substitution.  RESULTS: We describe a general method, based on a uniformization technique, which can be utilized to generate realizations of a Markovian substitution process conditional on an alignment of character states and a given tree topology. The method is applicable under a wide range of evolutionary models, and to illustrate its usefulness in practice, we embed it within a data augmentation-based Markov chain Monte Carlo sampler, for approximating posterior distributions under previously proposed codon substitution models. The sampler is found to be more efficient than the conventional pruning-based sampler with the decorrelation times between draws from the posterior reduced by a factor of 20 or more.},  Author = {Rodrigue, Nicolas and Philippe, Herv{\'e} and Lartillot, Nicolas},  Date-Added = {2014-07-07 10:22:52 +0000},  Date-Modified = {2014-07-07 10:24:58 +0000},  Doi = {10.1093/bioinformatics/btm532},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Mesh = {Algorithms; Bayes Theorem; Chromosome Mapping; Codon; Computer Simulation; Evolution, Molecular; Markov Chains; Models, Genetic; Models, Statistical; Pattern Recognition, Automated; Phylogeny; Sample Size; Sequence Alignment; Sequence Analysis, DNA},  Month = {Jan},  Number = {1},  Pages = {56-62},  Pmid = {18003644},  Pst = {ppublish},  Title = {Uniformization for sampling realizations of Markov processes: applications to Bayesian implementations of codon substitution models},  Volume = {24},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/btm532}}  @article{Oliveira2004,  Abstract = {A safe and effective HIV-1 vaccine is urgently needed to control the worldwide AIDS epidemic. Traditional methods of vaccine development have been frustratingly slow, and it is becoming increasingly apparent that radical new approaches may be required. Computational and mathematical approaches, combined with evolutionary reasoning, may provide new insights for the design of an efficacious AIDS vaccine. Here, we used codon-based substitution models and maximum-likelihood (ML) methods to identify positively selected sites that are likely to be involved in the immune control of HIV-1. Analysis of subtypes B and C revealed widespread adaptive evolution. Positively selected amino acids were detected in all nine HIV-1 proteins, including Env. Of particular interest was the high level of positive selection within the C-terminal regions of the immediate-early regulatory proteins, Tat and Rev. Many of the amino acid replacements were associated with the emergence of novel (or alternative) myristylation and casein kinase II (CKII) phosphorylation sites. The impact of these changes on the conformation and antigenicity of Tat and Rev remains to be established. In rhesus macaques, a single CTL-associated amino substitution in Tat has been linked to escape from acute SIV infection. Understanding the relationship between host-driven positive selection and antigenic variation may lead to the development of novel vaccine strategies that preempt the escape process.},  Author = {de Oliveira, Tulio and Salemi, Marco and Gordon, Michelle and Vandamme, Anne-Mieke and van Rensburg, Estrelita Janse and Engelbrecht, Susan and Coovadia, Hoosen M and Cassol, Sharon},  Date-Added = {2014-07-05 09:01:46 +0000},  Date-Modified = {2014-07-05 09:02:21 +0000},  Doi = {10.1534/genetics.103.018135},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Amino Acid Sequence; Chromosome Mapping; Databases, Genetic; Epitopes; Genes, rev; Genes, tat; Genetic Variation; Genome, Viral; HIV-1; Likelihood Functions; Models, Genetic; Molecular Sequence Data; Phylogeny; Selection, Genetic; Sequence Alignment; Vaccines},  Month = {Jul},  Number = {3},  Pages = {1047-58},  Pmc = {PMC1470929},  Pmid = {15280222},  Pst = {ppublish},  Title = {Mapping sites of positive selection and amino acid diversification in the HIV genome: an alternative approach to vaccine design?},  Volume = {167},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.103.018135}}  @article{Price1999,  Abstract = {Efforts to develop immune-based therapies for HIV infection have been impeded by incomplete definition of the immunological correlates of protection. Despite many precedents demonstrating that CD8(+) cytotoxic T lymphocytes are key mediators of protective anti-viral immunity in non-human animal models, direct evidence that these effector cells control viral replication in HIV-1 infection has remained elusive. The first part of this paper describes a detailed immunological and genetic study founded on evolutionary considerations. Following infection with HIV-1, virus variants which escaped recognition by autologous cytotoxic T lymphocytes were shown to possess a selection advantage within the host environment. Cytotoxic T lymphocytes therefore exert anti-viral pressure in vivo. This observation provides compelling evidence that cytotoxic T lymphocytes comprise a significant element of anti-retroviral immunity. Subsequently, the quantification of peripheral cytotoxic T lymphocyte frequencies utilizing peptide-(human leucocyte antigen class I) tetrameric complexes is described. Five patients with qualitatively similar immunodominant cytotoxic T lymphocyte responses during symptomatic primary HIV-1 infection were studied longitudinally. Expansions of virus-specific CD8(+) lymphocytes comprising up to 2% of the total CD8(+) T cell population were observed in the acute phase of infection. Antigenic load was identified as an important determinant of circulating HIV-1-specific CD8(+) lymphocyte levels; however, significant numbers of such cells were also found to persist following prolonged therapeutic suppression of plasma viraemia. In addition, an analysis of antigenic sequence variation with time in this case series suggests that the early administration of combination anti-retroviral therapy may limit HIV-1 mutational escape from host cytolytic specificities. The implications of these preliminary data are discussed. The data presented suggest that vaccination protocols should aim to elicit vigorous cytotoxic T lymphocyte responses to HIV-1. Attempts to stimulate polyvalent responses to mutationally intolerant epitopes are likely to be most effective. Optimal management of HIV-1 infection requires an understanding of dynamic host-virus interactions, and may involve strategies designed to enhance cytotoxic T lymphocyte activity following periods of anti-retroviral drug therapy.},  Author = {Price, D A and O'callaghan, C A and Whelan, J A and Easterbrook, P J and Phillips, R E},  Date-Added = {2014-07-05 09:01:00 +0000},  Date-Modified = {2014-07-05 09:01:24 +0000},  Journal = {Clin Sci (Lond)},  Journal-Full = {Clinical science (London, England : 1979)},  Mesh = {Acute Disease; Antigens, Viral; Antiviral Agents; HIV Infections; HIV-1; Humans; Lymphocyte Activation; Mutation; T-Lymphocytes, Cytotoxic; Time Factors; Virus Replication},  Month = {Dec},  Number = {6},  Pages = {707-18},  Pmid = {10585898},  Pst = {ppublish},  Title = {Cytotoxic T lymphocytes and viral evolution in primary HIV-1 infection},  Volume = {97},  Year = {1999}}  @article{Hu2000,  Abstract = {The evolution of human immunodeficiency virus type 1 infection is associated with a shift in the target cell population, driven by variability in coreceptor utilization resulting from diversity in env. To elucidate the potential consequences of these changes for Env-mediated fusion over the course of AIDS, we examined the biological properties of serial viral isolates and determined coreceptor utilization by the products of env cloned from two individuals, followed from the detection of seroconversion throughout the course of their infection. One had a typical course, and the other had an accelerated progression. Early isolates were non-syncytium inducing, and the corresponding Env exclusively utilized CCR5, whereas Env from late phases of infection showed restricted utilization of CXCR4 in both patients. Env from subject SC24, who had a standard progression, demonstrated multitropism, manifested by utilization of CCR3, CXCR4, and CCR5 in the intervening period. In contrast, Env from patient SC51, who experienced early conversion to the syncytium-inducing phenotype, developed dualtropic coreceptor utilization of CCR5 and CXCR4. Genetic analysis of env from each isolate revealed that those with an X4 phenotype formed a distinct subcluster within each subject. Analysis of chimeras constructed from R5 and multispecific env from patient SC24 demonstrated that while the V3 domain played a dominant role in determining coreceptor utilization, sequences in the V4-V5 region also contributed to the latter phenotype. Immunoprecipitation experiments confirmed that the hybrid Env proteins were expressed at similar levels. These experiments demonstrate that progression from the R5 to X4 phenotype may occur through a multi- or dual-tropic intermediate and that multiple domains contribute to this process.},  Author = {Hu, Q X and Barry, A P and Wang, Z X and Connolly, S M and Peiper, S C and Greenberg, M L},  Date-Added = {2014-07-05 08:59:52 +0000},  Date-Modified = {2014-07-05 09:00:17 +0000},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Acquired Immunodeficiency Syndrome; Amino Acid Sequence; Evolution, Molecular; Gene Expression Regulation, Viral; Genome, Viral; HIV-1; Humans; Molecular Sequence Data; Phylogeny; Receptors, Virus; Viral Envelope Proteins},  Month = {Dec},  Number = {24},  Pages = {11858-72},  Pmc = {PMC112469},  Pmid = {11090186},  Pst = {ppublish},  Title = {Evolution of the human immunodeficiency virus type 1 envelope during infection reveals molecular corollaries of specificity for coreceptor utilization and AIDS pathogenesis},  Volume = {74},  Year = {2000}}  @article{Finzi1999,  Abstract = {Combination therapy for HIV-1 infection can reduce plasma virus to undetectable levels, indicating that prolonged treatment might eradicate the infection. However, HIV-1 can persist in a latent form in resting CD4+ T cells. We measured the decay rate of this latent reservoir in 34 treated adults whose plasma virus levels were undetectable. The mean half-life of the latent reservoir was very long (43.9 months). If the latent reservoir consists of only 1 x 10(5) cells, eradication could take as long as 60 years. Thus, latent infection of resting CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective anti-retroviral therapy.},  Author = {Finzi, D and Blankson, J and Siliciano, J D and Margolick, J B and Chadwick, K and Pierson, T and Smith, K and Lisziewicz, J and Lori, F and Flexner, C and Quinn, T C and Chaisson, R E and Rosenberg, E and Walker, B and Gange, S and Gallant, J and Siliciano, R F},  Date-Added = {2014-07-05 08:58:30 +0000},  Date-Modified = {2014-07-05 08:58:55 +0000},  Doi = {10.1038/8394},  Journal = {Nat Med},  Journal-Full = {Nature medicine},  Mesh = {Adult; CD4-Positive T-Lymphocytes; Cells, Cultured; Cross-Sectional Studies; Drug Therapy, Combination; Female; HIV Infections; HIV-1; Half-Life; Humans; Longitudinal Studies; Male; Middle Aged; RNA, Viral; Viral Load; Virus Latency; Virus Replication},  Month = {May},  Number = {5},  Pages = {512-7},  Pmid = {10229227},  Pst = {ppublish},  Title = {Latent infection of CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective combination therapy},  Volume = {5},  Year = {1999},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/8394}}  @article{Lakner2008,  Abstract = {The main limiting factor in Bayesian MCMC analysis of phylogeny is typically the efficiency with which topology proposals sample tree space. Here we evaluate the performance of seven different proposal mechanisms, including most of those used in current Bayesian phylogenetics software. We sampled 12 empirical nucleotide data sets--ranging in size from 27 to 71 taxa and from 378 to 2,520 sites--under difficult conditions: short runs, no Metropolis-coupling, and an oversimplified substitution model producing difficult tree spaces (Jukes Cantor with equal site rates). Convergence was assessed by comparison to reference samples obtained from multiple Metropolis-coupled runs. We find that proposals producing topology changes as a side effect of branch length changes (LOCAL and Continuous Change) consistently perform worse than those involving stochastic branch rearrangements (nearest neighbor interchange, subtree pruning and regrafting, tree bisection and reconnection, or subtree swapping). Among the latter, moves that use an extension mechanism to mix local with more distant rearrangements show better overall performance than those involving only local or only random rearrangements. Moves with only local rearrangements tend to mix well but have long burn-in periods, whereas moves with random rearrangements often show the reverse pattern. Combinations of moves tend to perform better than single moves. The time to convergence can be shortened considerably by starting with a good tree, but this comes at the cost of compromising convergence diagnostics based on overdispersed starting points. Our results have important implications for developers of Bayesian MCMC implementations and for the large group of users of Bayesian phylogenetics software.},  Author = {Lakner, Clemens and van der Mark, Paul and Huelsenbeck, John P and Larget, Bret and Ronquist, Fredrik},  Date-Added = {2014-07-03 00:22:51 +0000},  Date-Modified = {2014-07-04 01:55:04 +0000},  Doi = {10.1080/10635150801886156},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Mesh = {Bayes Theorem; Markov Chains; Models, Genetic; Monte Carlo Method; Phylogeny},  Month = {2},  Number = {1},  Pages = {86-103},  Pmid = {18278678},  Pst = {ppublish},  Title = {Efficiency of Markov chain Monte Carlo tree proposals in Bayesian phylogenetics},  Volume = {57},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1080/10635150801886156}}  @article{nylander2008awty,  Author = {Nylander, Johan A A and Wilgenbusch, James C and Warren, Dan L and Swofford, David L},  Date-Added = {2014-07-03 00:04:43 +0000},  Date-Modified = {2014-07-06 03:17:16 +0000},  Journal = {Bioinformatics},  Number = {4},  Pages = {581--583},  Publisher = {Oxford Univ Press},  Title = {AWTY (are we there yet?): a system for graphical exploration of MCMC convergence in Bayesian phylogenetics},  Volume = {24},  Year = {2008}}  @article{HohnaDrummond2012,  Author = {H{\"o}hna, Sebastian and Drummond, Alexei J},  Date-Added = {2014-07-03 00:00:19 +0000},  Date-Modified = {2014-07-05 08:50:44 +0000},  Doi = {10.1093/sysbio/syr074},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Mesh = {Algorithms; Bayes Theorem; Classification; Data Interpretation, Statistical; Markov Chains; Models, Genetic; Monte Carlo Method; Phylogeny; Probability},  Month = {1},  Number = {1},  Pages = {1-11},  Pmid = {21828081},  Pst = {ppublish},  Title = {Guided tree topology proposals for Bayesian phylogenetic inference},  Volume = {61},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/syr074}}  @article{whidden2014quantifying,  Author = {Whidden, Christopher and Matsen, IV and Frederick, A},  Date-Added = {2014-07-02 03:01:56 +0000},  Date-Modified = {2014-07-02 03:01:56 +0000},  Journal = {arXiv preprint arXiv:1405.2120},  Title = {Quantifying MCMC Exploration of Phylogenetic Tree Space},  Year = {2014}}  @article{gavryushkina2014bayesian,  Author = {Gavryushkina, Alexandra and Welch, David and Stadler, Tanja and Drummond, Alexei J.},  Date-Added = {2014-06-25 21:51:42 +0000},  Date-Modified = {2014-07-06 00:53:22 +0000},  Journal = {arXiv preprint arXiv:1406.4573},  Title = {Bayesian inference of sampled ancestor trees for epidemiology and fossil calibration},  Year = {2014}}  @inbook{RodrigoFelsenstein1999,  Author = {Rodrigo, A. G. and Felsenstein, J.},  Chapter = {{Coalescent approaches to HIV population genetics}},  Date-Added = {2014-06-25 21:40:21 +0000},  Date-Modified = {2014-07-06 01:00:48 +0000},  Pages = {233--272},  Publisher = {The Johns Hopkins University Press},  Title = {The evolution of {HIV}},  Year = {1999}}  @article{Gillespie:2001wj,  Abstract = {This paper examines aspects of genetic draft, the stochastic force induced by substitutions at one locus on the dynamics of a closely linked locus. Of particular interest is the role of population size on genetic draft. Remarkably, the rate of substitution of weakly selected advantageous mutations decreases with increasing population size, whereas that for deleterious mutations increases with population size. This dependency on population size is the opposite of that for genetic drift. Moreover, these rates are only weakly dependent on population size, again contrary to the strong dependency of drift-based dynamics. Four models of the strongly selected loci responsible for genetic draft are examined. Three of these exhibit a very weak dependency on population size, which implies that their induced effects will also be weakly dependent on population size. Together, these results suggest that population size and binomial sampling may not be relevant to a species' evolution. If this is the case, then a number of evolutionary conundrums are resolved.},  Author = {Gillespie, J H},  Date-Added = {2014-05-23 01:56:00 +0000},  Date-Modified = {2014-07-04 01:54:16 +0000},  Journal = {Evolution},  Journal-Full = {Evolution; international journal of organic evolution},  Mesh = {Alleles; Animals; Biological Evolution; Genetics, Population; Genotype; Mathematics; Mutation; Phenotype; Population Density},  Month = {11},  Number = {11},  Pages = {2161-9},  Pmid = {11794777},  Pst = {ppublish},  Title = {Is the population size of a species relevant to its evolution?},  Volume = {55},  Year = {2001}}  @article{Wakeley2009,  Abstract = {We suggest two extensions of the coalescent effective population size of Sj{\"o}din et al. (2005) and make a third, practical point. First, to bolster its relevance to data and allow comparisons between models, the coalescent effective size should be recast as a kind of mutation effective size. Second, the requirement that the coalescent effective population size must depend linearly on the actual population size should be lifted. Third, even if the coalescent effective population size does not exist in the mathematical sense, it may be difficult to reject Kingman's coalescent using genetic data.},  Author = {Wakeley, John and Sargsyan, Ori},  Date-Added = {2014-05-22 04:10:39 +0000},  Date-Modified = {2014-07-04 02:00:19 +0000},  Doi = {10.1534/genetics.108.092460},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Animals; Models, Genetic; Population Density},  Month = {1},  Number = {1},  Pages = {341-5},  Pmc = {PMC2621185},  Pmid = {19001293},  Pst = {ppublish},  Title = {Extensions of the coalescent effective population size},  Volume = {181},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.108.092460}}  @article{Sjodin2005,  Abstract = {We investigate conditions under which a model with stochastic demography or population structure converges to the coalescent with a linear change in timescale. We argue that this is a necessary condition for the existence of a meaningful effective population size. We find that such a linear timescale change is obtained when demographic fluctuations and coalescence events occur on different timescales. Simple models of population structure and randomly fluctuating population size are used to exemplify the ideas and provide an intuitive feel for the meaning of the conditions.},  Author = {Sj{\"o}din, P and Kaj, I and Krone, S and Lascoux, M and Nordborg, M},  Date-Added = {2014-05-22 04:08:47 +0000},  Date-Modified = {2014-07-04 01:58:21 +0000},  Doi = {10.1534/genetics.104.026799},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Computer Simulation; Demography; Genetics, Population; Markov Chains; Models, Genetic; Models, Theoretical; Population Density; Population Dynamics; Stochastic Processes; Time Factors},  Month = {2},  Number = {2},  Pages = {1061-70},  Pmc = {PMC1449138},  Pmid = {15489538},  Pst = {ppublish},  Title = {On the meaning and existence of an effective population size},  Volume = {169},  Year = {2005},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.104.026799}}  @article{Bouckaert2014,  Abstract = {We present a new open source, extensible and flexible software platform for Bayesian evolutionary analysis called BEAST 2. This software platform is a re-design of the popular BEAST 1 platform to correct structural deficiencies that became evident as the BEAST 1 software evolved. Key among those deficiencies was the lack of post-deployment extensibility. BEAST 2 now has a fully developed package management system that allows third party developers to write additional functionality that can be directly installed to the BEAST 2 analysis platform via a package manager without requiring a new software release of the platform. This package architecture is showcased with a number of recently published new models encompassing birth-death-sampling tree priors, phylodynamics and model averaging for substitution models and site partitioning. A second major improvement is the ability to read/write the entire state of the MCMC chain to/from disk allowing it to be easily shared between multiple instances of the BEAST software. This facilitates checkpointing and better support for multi-processor and high-end computing extensions. Finally, the functionality in new packages can be easily added to the user interface (BEAUti 2) by a simple XML template-based mechanism because BEAST 2 has been re-designed to provide greater integration between the analysis engine and the user interface so that, for example BEAST and BEAUti use exactly the same XML file format.},  Author = {Bouckaert, Remco R. and Heled, Joseph and K{\"u}hnert, Denise and Vaughan, Tim and Wu, Chieh-Hsi and Xie, Dong and Suchard, Marc A and Rambaut, Andrew and Drummond, Alexei J},  Date-Added = {2014-05-21 03:24:22 +0000},  Date-Modified = {2014-07-06 03:46:41 +0000},  Doi = {10.1371/journal.pcbi.1003537},  Journal = {PLoS Comput Biol},  Journal-Full = {PLoS computational biology},  Month = {Apr},  Number = {4},  Pages = {e1003537},  Pmc = {PMC3985171},  Pmid = {24722319},  Pst = {epublish},  Title = {BEAST 2: a software platform for Bayesian evolutionary analysis},  Volume = {10},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.1003537}}  @article{PybusRambaut2002,  Abstract = {UNLABELLED: GENIE implements a statistical framework for inferring the demographic history of a population from phylogenies that have been reconstructed from sampled DNA sequences. The methods are based on population genetic models known collectively as coalescent theory.  AVAILABILITY: GENIE is available from http://evolve.zoo.ox.ac.uk. All popular operating systems are supported.},  Author = {Pybus, O G and Rambaut, A},  Date-Added = {2014-05-13 03:56:49 +0000},  Date-Modified = {2014-07-04 01:56:08 +0000},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Mesh = {Computer Simulation; Database Management Systems; Demography; Evolution, Molecular; Genetics, Population; Information Storage and Retrieval; Models, Genetic; Models, Statistical; Pedigree; Phylogeny; Population Dynamics; Software},  Month = {10},  Number = {10},  Pages = {1404-5},  Pmid = {12376389},  Pst = {ppublish},  Title = {GENIE: estimating demographic history from molecular phylogenies},  Volume = {18},  Year = {2002}}  @article{SlatkinHudson1991,  Author = {Slatkin, M and Hudson, R R},  Date-Added = {2014-05-05 04:15:36 +0000},  Date-Modified = {2014-07-05 08:51:04 +0000},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Animals; Base Sequence; DNA, Mitochondrial; Genetic Variation; Humans; Mathematics; Models, Genetic; Population Growth; Sequence Homology, Nucleic Acid},  Month = {Oct},  Number = {2},  Pages = {555-62},  Pmc = {PMC1204643},  Pmid = {1743491},  Pst = {ppublish},  Title = {Pairwise comparisons of mitochondrial DNA sequences in stable and exponentially growing populations},  Volume = {129},  Year = {1991}}  @article{vaughan2014efficient,  Author = {Vaughan, T. G. and K{\"u}hnert, D and Popinga, A and Welch, D and Drummond, A. J.},  Date-Added = {2014-05-05 04:04:28 +0000},  Date-Modified = {2014-07-06 00:52:28 +0000},  Journal = {Bioinformatics},  Pages = {btu201},  Publisher = {Oxford Univ Press},  Title = {Efficient Bayesian inference under the structured coalescent},  Year = {2014}}  @article{irvahn2014phylogenetic,  Author = {Irvahn, Jan and Minin, Vladimir N},  Date-Added = {2014-05-05 04:03:30 +0000},  Date-Modified = {2014-05-05 04:03:30 +0000},  Journal = {arXiv preprint arXiv:1403.5040},  Title = {Phylogenetic Stochastic Mapping without Matrix Exponentiation},  Year = {2014}}  @article{Lemey:2014eu,  Abstract = {Information on global human movement patterns is central to spatial epidemiological models used to predict the behavior of influenza and other infectious diseases. Yet it remains difficult to test which modes of dispersal drive pathogen spread at various geographic scales using standard epidemiological data alone. Evolutionary analyses of pathogen genome sequences increasingly provide insights into the spatial dynamics of influenza viruses, but to date they have largely neglected the wealth of information on human mobility, mainly because no statistical framework exists within which viral gene sequences and empirical data on host movement can be combined. Here, we address this problem by applying a phylogeographic approach to elucidate the global spread of human influenza subtype H3N2 and assess its ability to predict the spatial spread of human influenza A viruses worldwide. Using a framework that estimates the migration history of human influenza while simultaneously testing and quantifying a range of potential predictive variables of spatial spread, we show that the global dynamics of influenza H3N2 are driven by air passenger flows, whereas at more local scales spread is also determined by processes that correlate with geographic distance. Our analyses further confirm a central role for mainland China and Southeast Asia in maintaining a source population for global influenza diversity. By comparing model output with the known pandemic expansion of H1N1 during 2009, we demonstrate that predictions of influenza spatial spread are most accurate when data on human mobility and viral evolution are integrated. In conclusion, the global dynamics of influenza viruses are best explained by combining human mobility data with the spatial information inherent in sampled viral genomes. The integrated approach introduced here offers great potential for epidemiological surveillance through phylogeographic reconstructions and for improving predictive models of disease control.},  Author = {Lemey, Philippe and Rambaut, Andrew and Bedford, Trevor and Faria, Nuno and Bielejec, Filip and Baele, Guy and Russell, Colin A and Smith, Derek J and Pybus, Oliver G and Brockmann, Dirk and Suchard, Marc A},  Date-Added = {2014-05-05 04:00:11 +0000},  Date-Modified = {2014-05-05 04:00:11 +0000},  Doi = {10.1371/journal.ppat.1003932},  Journal = {PLoS Pathog},  Journal-Full = {PLoS pathogens},  Month = {Feb},  Number = {2},  Pages = {e1003932},  Pmc = {PMC3930559},  Pmid = {24586153},  Pst = {epublish},  Title = {Unifying viral genetics and human transportation data to predict the global transmission dynamics of human influenza H3N2},  Volume = {10},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.ppat.1003932}}  @article{Szollosi:2013ly,  Abstract = {In phylogenetic studies, the evolution of molecular sequences is assumed to have taken place along the phylogeny traced by the ancestors of extant species. In the presence of lateral gene transfer, however, this may not be the case, because the species lineage from which a gene was transferred may have gone extinct or not have been sampled. Because it is not feasible to specify or reconstruct the complete phylogeny of all species, we must describe the evolution of genes outside the represented phylogeny by modeling the speciation dynamics that gave rise to the complete phylogeny. We demonstrate that if the number of sampled species is small compared with the total number of existing species, the overwhelming majority of gene transfers involve speciation to and evolution along extinct or unsampled lineages. We show that the evolution of genes along extinct or unsampled lineages can to good approximation be treated as those of independently evolving lineages described by a few global parameters. Using this result, we derive an algorithm to calculate the probability of a gene tree and recover the maximum-likelihood reconciliation given the phylogeny of the sampled species. Examining 473 near-universal gene families from 36 cyanobacteria, we find that nearly a third of transfer events (28%) appear to have topological signatures of evolution along extinct species, but only approximately 6% of transfers trace their ancestry to before the common ancestor of the sampled cyanobacteria.},  Author = {Sz{\"o}llosi, Gergely J and Tannier, Eric and Lartillot, Nicolas and Daubin, Vincent},  Date-Added = {2014-05-05 03:58:46 +0000},  Date-Modified = {2014-05-05 03:58:46 +0000},  Doi = {10.1093/sysbio/syt003},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Mesh = {Algorithms; Biodiversity; Biological Evolution; Cyanobacteria; DNA, Bacterial; Evolution, Molecular; Gene Transfer, Horizontal; Genes, Bacterial; Genetic Speciation; Models, Genetic; Phylogeny; Sequence Analysis, DNA},  Month = {May},  Number = {3},  Pages = {386-97},  Pmc = {PMC3622898},  Pmid = {23355531},  Pst = {ppublish},  Title = {Lateral gene transfer from the dead},  Volume = {62},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/syt003}}  @article{Szollosi:2012rz,  Abstract = {The timing of the evolution of microbial life has largely remained elusive due to the scarcity of prokaryotic fossil record and the confounding effects of the exchange of genes among possibly distant species. The history of gene transfer events, however, is not a series of individual oddities; it records which lineages were concurrent and thus provides information on the timing of species diversification. Here, we use a probabilistic model of genome evolution that accounts for differences between gene phylogenies and the species tree as series of duplication, transfer, and loss events to reconstruct chronologically ordered species phylogenies. Using simulations we show that we can robustly recover accurate chronologically ordered species phylogenies in the presence of gene tree reconstruction errors and realistic rates of duplication, transfer, and loss. Using genomic data we demonstrate that we can infer rooted species phylogenies using homologous gene families from complete genomes of 10 bacterial and archaeal groups. Focusing on cyanobacteria, distinguished among prokaryotes by a relative abundance of fossils, we infer the maximum likelihood chronologically ordered species phylogeny based on 36 genomes with 8,332 homologous gene families. We find the order of speciation events to be in full agreement with the fossil record and the inferred phylogeny of cyanobacteria to be consistent with the phylogeny recovered from established phylogenomics methods. Our results demonstrate that lateral gene transfers, detected by probabilistic models of genome evolution, can be used as a source of information on the timing of evolution, providing a valuable complement to the limited prokaryotic fossil record.},  Author = {Sz{\"o}llosi, Gergely J and Boussau, Bastien and Abby, Sophie S and Tannier, Eric and Daubin, Vincent},  Date-Added = {2014-05-05 03:56:40 +0000},  Date-Modified = {2014-05-05 03:56:40 +0000},  Doi = {10.1073/pnas.1202997109},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Gene Transfer, Horizontal; Likelihood Functions; Models, Genetic; Phylogeny; Species Specificity},  Month = {Oct},  Number = {43},  Pages = {17513-8},  Pmc = {PMC3491530},  Pmid = {23043116},  Pst = {ppublish},  Title = {Phylogenetic modeling of lateral gene transfer reconstructs the pattern and relative timing of speciations},  Volume = {109},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.1202997109}}  @article{Sjostrand:2014rt,  Abstract = {Lateral gene transfer (LGT)-which transfers DNA between two non-vertically related individuals belonging to the same or different species-is recognized as a major force in prokaryotic evolution, and evidence of its impact on eukaryotic evolution is ever increasing. LGT has attracted much public attention for its potential to transfer pathogenic elements and antibiotic resistance in bacteria, and to transfer pesticide resistance from genetically modified crops to other plants. In a wider perspective, there is a growing body of studies highlighting the role of LGT in enabling organisms to occupy new niches or adapt to environmental changes. The challenge LGT poses to the standard tree-based conception of evolution is also being debated. Studies of LGT have, however, been severely limited by a lack of computational tools. The best currently available LGT algorithms are parsimony-based phylogenetic methods, which require a pre-computed gene tree and cannot choose between sometimes wildly differing most parsimonious solutions. Moreover, in many studies, simple heuristics are applied that can only handle putative orthologs and completely disregard gene duplications (GDs). Consequently, proposed LGT among specific gene families, and the rate of LGT in general, remain debated. We present a Bayesian Markov-chain Monte Carlo-based method that integrates GD, gene loss, LGT, and sequence evolution, and apply the method in a genome-wide analysis of two groups of bacteria: Mollicutes and Cyanobacteria. Our analyses show that although the LGT rate between distant species is high, the net combined rate of duplication and close-species LGT is on average higher. We also show that the common practice of disregarding reconcilability in gene tree inference overestimates the number of LGT and duplication events. [Bayesian; gene duplication; gene loss; horizontal gene transfer; lateral gene transfer; MCMC; phylogenetics.].},  Author = {Sj{\"o}strand, Joel and Tofigh, Ali and Daubin, Vincent and Arvestad, Lars and Sennblad, Bengt and Lagergren, Jens},  Date-Added = {2014-05-05 03:55:43 +0000},  Date-Modified = {2014-05-05 03:55:43 +0000},  Doi = {10.1093/sysbio/syu007},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Month = {May},  Number = {3},  Pages = {409-20},  Pmid = {24562812},  Pst = {ppublish},  Title = {A bayesian method for analyzing lateral gene transfer},  Volume = {63},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/syu007}}  @article{jones2014dissect,  Author = {Jones, Graham and Oxelman, Bengt},  Date-Added = {2014-05-05 03:54:45 +0000},  Date-Modified = {2014-05-05 03:54:45 +0000},  Title = {DISSECT: an assignment-free Bayesian discovery method for},  Year = {2014}}  @article{szollosi2013inference,  Author = {Sz{\"o}llosi, Gergely J and Tannier, Eric and Daubin, Vincent and Boussau, Bastien},  Date-Added = {2014-05-05 03:52:57 +0000},  Date-Modified = {2014-05-05 03:52:57 +0000},  Journal = {arXiv preprint arXiv:1311.0651},  Title = {The inference of gene trees with species trees},  Year = {2013}}  @article{Hartfield2014,  Author = {Hartfield, Matthew and Murall, Carmen L{\'\i}a and Alizon, Samuel},  Date-Added = {2014-05-05 03:51:47 +0000},  Date-Modified = {2014-05-05 03:51:47 +0000},  Doi = {http://dx.doi.org/10.1016/j.molmed.2014.04.002},  Issn = {1471-4914},  Journal = {Trends in Molecular Medicine},  Keywords = {\{HCV\}},  Number = {0},  Pages = {-},  Title = {Clinical applications of pathogen phylogenies},  Url = {http://www.sciencedirect.com/science/article/pii/S147149141400063X},  Year = {2014},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S147149141400063X},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.molmed.2014.04.002}}  @article{Silvestro:2014kx,  Abstract = {The temporal dynamics of species diversity are shaped by variations in the rates of speciation and extinction, and there is a long history of inferring these rates using first and last appearances of taxa in the fossil record. Understanding diversity dynamics critically depends on unbiased estimates of the unobserved times of speciation and extinction for all lineages, but the inference of these parameters is challenging due to the complex nature of the available data. Here, we present a new probabilistic framework to jointly estimate species-specific times of speciation and extinction and the rates of the underlying birth-death process based on the fossil record. The rates are allowed to vary through time independently of each other, and the probability of preservation and sampling is explicitly incorporated in the model to estimate the true lifespan of each lineage. We implement a Bayesian algorithm to assess the presence of rate shifts by exploring alternative diversification models. Tests on a range of simulated data sets reveal the accuracy and robustness of our approach against violations of the underlying assumptions and various degrees of data incompleteness. Finally, we demonstrate the application of our method with the diversification of the mammal family Rhinocerotidae and reveal a complex history of repeated and independent temporal shifts of both speciation and extinction rates, leading to the expansion and subsequent decline of the group. The estimated parameters of the birth-death process implemented here are directly comparable with those obtained from dated molecular phylogenies. Thus, our model represents a step towards integrating phylogenetic and fossil information to infer macroevolutionary processes.[BDMCMC; biodiversity trends; Birth-death process; incomplete fossil sampling; macroevolution; species rise and fall.].},  Author = {Silvestro, Daniele and Schnitzler, Jan and Liow, Lee Hsiang and Antonelli, Alexandre and Salamin, Nicolas},  Date-Added = {2014-05-05 03:34:15 +0000},  Date-Modified = {2014-05-05 03:34:15 +0000},  Doi = {10.1093/sysbio/syu006},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Month = {May},  Number = {3},  Pages = {349-67},  Pmid = {24510972},  Pst = {ppublish},  Title = {Bayesian estimation of speciation and extinction from incomplete fossil occurrence data},  Volume = {63},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/syu006}}  @article{dos2014impact,  Author = {Dos Reis, Mario and Zhu, Tianqi and Yang, Ziheng},  Date-Added = {2014-05-05 03:32:43 +0000},  Date-Modified = {2014-05-05 03:32:49 +0000},  Journal = {Systematic biology},  Pages = {syu020},  Publisher = {Oxford University Press},  Title = {The Impact of the Rate Prior on Bayesian Estimation of Divergence Times with Multiple Loci},  Year = {2014}}  @article{steel2014tracing,  Author = {Steel, Mike},  Date-Added = {2014-05-05 03:24:30 +0000},  Date-Modified = {2014-05-05 03:24:44 +0000},  Journal = {arXiv preprint arXiv:1402.3771},  Title = {Tracing evolutionary links between species},  Year = {2014}}  @article{Kuhnert:2014uq,  Abstract = {The evolution of RNA viruses, such as human immunodeficiency virus (HIV), hepatitis C virus and influenza virus, occurs so rapidly that the viruses' genomes contain information on past ecological dynamics. Hence, we develop a phylodynamic method that enables the joint estimation of epidemiological parameters and phylogenetic history. Based on a compartmental susceptible-infected-removed (SIR) model, this method provides separate information on incidence and prevalence of infections. Detailed information on the interaction of host population dynamics and evolutionary history can inform decisions on how to contain or entirely avoid disease outbreaks. We apply our birth-death SIR method to two viral datasets. First, five HIV type 1 clusters sampled in the UK between 1999 and 2003 are analysed. The estimated basic reproduction ratios range from 1.9 to 3.2 among the clusters. All clusters show a decline in the growth rate of the local epidemic in the middle or end of the 1990s. The analysis of a hepatitis C virus genotype 2c dataset shows that the local epidemic in the C{\'o}rdoban city Cruz del Eje originated around 1906 (median), coinciding with an immigration wave from Europe to central Argentina that dates from 1880 to 1920. The estimated time of epidemic peak is around 1970.},  Author = {K{\"u}hnert, Denise and Stadler, Tanja and Vaughan, Timothy G and Drummond, Alexei J},  Date-Added = {2014-03-13 22:27:33 +0000},  Date-Modified = {2014-03-13 22:27:33 +0000},  Doi = {10.1098/rsif.2013.1106},  Journal = {J R Soc Interface},  Journal-Full = {Journal of the Royal Society, Interface / the Royal Society},  Keywords = {Bayesian phylogenetics; birth--death prior; mathematical epidemiology; phylodynamics},  Number = {94},  Pages = {20131106},  Pmid = {24573331},  Pst = {epublish},  Title = {Simultaneous reconstruction of evolutionary history and epidemiological dynamics from viral sequences with the birth-death SIR model},  Volume = {11},  Year = {2014},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rsif.2013.1106}}  @article{Ypma:2013fk,  Abstract = {Transmission events are the fundamental building blocks of the dynamics of any infectious disease. Much about the epidemiology of a disease can be learned when these individual transmission events are known or can be estimated. Such estimations are difficult and generally feasible only when detailed epidemiological data are available. The genealogy estimated from genetic sequences of sampled pathogens is another rich source of information on transmission history. Optimal inference of transmission events calls for the combination of genetic data and epidemiological data into one joint analysis. A key difficulty is that the transmission tree, which describes the transmission events between infected hosts, differs from the phylogenetic tree, which describes the ancestral relationships between pathogens sampled from these hosts. The trees differ both in timing of the internal nodes and in topology. These differences become more pronounced when a higher fraction of infected hosts is sampled. We show how the phylogenetic tree of sampled pathogens is related to the transmission tree of an outbreak of an infectious disease, by the within-host dynamics of pathogens. We provide a statistical framework to infer key epidemiological and mutational parameters by simultaneously estimating the phylogenetic tree and the transmission tree. We test the approach using simulations and illustrate its use on an outbreak of foot-and-mouth disease. The approach unifies existing methods in the emerging field of phylodynamics with transmission tree reconstruction methods that are used in infectious disease epidemiology.},  Author = {Ypma, Rolf J F and van Ballegooijen, W Marijn and Wallinga, Jacco},  Date-Added = {2014-03-13 22:23:09 +0000},  Date-Modified = {2014-07-04 02:00:29 +0000},  Doi = {10.1534/genetics.113.154856},  Journal = {Genetics},  Journal-Full = {Genetics},  Keywords = {Markov chain Monte Carlo (MCMC); foot-and-mouth disease; molecular epidemiology; transmission tree},  Month = {11},  Number = {3},  Pages = {1055-62},  Pmc = {PMC3813836},  Pmid = {24037268},  Pst = {ppublish},  Title = {Relating phylogenetic trees to transmission trees of infectious disease outbreaks},  Volume = {195},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.113.154856}}  @article{Kendall:1949uq,  Author = {Kendall, David G.},  Date-Added = {2013-10-31 16:30:03 +0000},  Date-Modified = {2013-10-31 16:30:03 +0000},  Journal = {Journal of the Royal Statistical Society. Series B (Methodological)},  Number = {2},  Pages = {230--282},  Publisher = {JSTOR},  Title = {Stochastic processes and population growth},  Volume = {11},  Year = {1949}}  @article{leventhal2013using,  Author = {Leventhal, G. E. and Guenthard, H.F. and Bonhoeffer, S. and Stadler, Tanja},  Date-Added = {2013-08-30 03:50:27 +0000},  Date-Modified = {2013-08-30 04:05:35 +0000},  Journal = {Mol Biol Evol},  Title = {Using an epidemiological model for phylogenetic inference reveals density-dependence in {HIV} transmission},  Volume = {in press},  Year = {2013}}  @article{beaumont2010defence,  Author = {Beaumont, Mark A and Nielsen, Rasmus and Robert, Christian and Hey, Jody and Gaggiotti, Oscar and Knowles, Lacey and Estoup, Arnaud and Panchal, Mahesh and Corander, Jukka and Hickerson, Mike},  Date-Added = {2013-08-11 20:30:10 +0000},  Date-Modified = {2013-08-11 20:31:19 +0000},  Journal = {Molecular Ecology},  Number = {3},  Pages = {436--446},  Title = {In defence of model-based inference in phylogeography},  Volume = {19},  Year = {2010}}  @article{Coop:2004uq,  Abstract = {The extent to which natural selection shapes diversity within populations is a key question for population genetics. Thus, there is considerable interest in quantifying the strength of selection. A full likelihood approach for inference about selection at a single site within an otherwise neutral fully linked sequence of sites is described here. A coalescent model of evolution is used to model the ancestry of a sample of DNA sequences which have the selected site segregating. The mutation model, for the selected and neutral sites, is the infinitely many-sites model where there is no back or parallel mutation at sites. A unique perfect phylogeny, a gene tree, can be constructed from the configuration of mutations on the sample sequences under this model of mutation. The approach is general and can be used for any bi-allelic selection scheme. Selection is incorporated through modelling the frequency of the selected and neutral allelic classes stochastically back in time, then using a subdivided population model considering the population frequencies through time as variable population sizes. An importance sampling algorithm is then used to explore over coalescent tree space consistent with the data. The method is applied to a simulated data set and the gene tree presented in Verrelli et al. (2002).},  Author = {Coop, Graham and Griffiths, Robert C},  Date-Added = {2013-08-11 05:06:05 +0000},  Date-Modified = {2013-08-11 05:06:05 +0000},  Doi = {10.1016/j.tpb.2004.06.006},  Journal = {Theor Popul Biol},  Journal-Full = {Theoretical population biology},  Mesh = {Genetic Variation; Likelihood Functions; Mutation; Selection, Genetic},  Month = {Nov},  Number = {3},  Pages = {219-32},  Pmid = {15465123},  Pst = {ppublish},  Title = {Ancestral inference on gene trees under selection},  Volume = {66},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tpb.2004.06.006}}  @article{Palmer:2013fk,  Abstract = {The rates of escape and reversion in response to selection pressure arising from the host immune system, notably the cytotoxic T-lymphocyte (CTL) response, are key factors determining the evolution of HIV. Existing methods for estimating these parameters from cross-sectional population data using ordinary differential equations (ODEs) ignore information about the genealogy of sampled HIV sequences, which has the potential to cause systematic bias and overestimate certainty. Here, we describe an integrated approach, validated through extensive simulations, which combines genealogical inference and epidemiological modelling, to estimate rates of CTL escape and reversion in HIV epitopes. We show that there is substantial uncertainty about rates of viral escape and reversion from cross-sectional data, which arises from the inherent stochasticity in the evolutionary process. By application to empirical data, we find that point estimates of rates from a previously published ODE model and the integrated approach presented here are often similar, but can also differ several-fold depending on the structure of the genealogy. The model-based approach we apply provides a framework for the statistical analysis and hypothesis testing of escape and reversion in population data and highlights the need for longitudinal and denser cross-sectional sampling to enable accurate estimate of these key parameters.},  Author = {Palmer, Duncan and Frater, John and Phillips, Rodney and McLean, Angela R and McVean, Gil},  Date-Added = {2013-08-11 00:23:42 +0000},  Date-Modified = {2013-08-11 00:23:42 +0000},  Doi = {10.1098/rspb.2013.0696},  Journal = {Proc Biol Sci},  Journal-Full = {Proceedings. Biological sciences / The Royal Society},  Keywords = {HIV; cytotoxic T-lymphocyte; escape; genealogy; peeling; phylodynamics},  Month = {Jul},  Number = {1762},  Pages = {20130696},  Pmc = {PMC3673055},  Pmid = {23677344},  Pst = {epublish},  Title = {Integrating genealogical and dynamical modelling to infer escape and reversion rates in HIV epitopes},  Volume = {280},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rspb.2013.0696}}  @article{MASTER,  Abstract = {In this article, we present a versatile new software tool for the simulation and analysis of stochastic models of population phylodynamics and chemical kinetics. Models are specified via an expressive and human-readable XML format and can be used as the basis for generating either single population histories or large ensembles of such histories. Importantly, phylogenetic trees or networks can be generated alongside the histories they correspond to, enabling investigations into the interplay between genealogies and population dynamics. Summary statistics such as means and variances can be recorded in place of the full ensemble, allowing for a reduction in the amount of memory used--an important consideration for models including large numbers of individual subpopulations or demes. In the case of population size histories, the resulting simulation output is written to disk in the flexible JSON format, which is easily read into numerical analysis environments such as R for visualization or further processing. Simulated phylogenetic trees can be recorded using the standard Newick or NEXUS formats, with extensions to these formats used for non-tree-like inheritance relationships.},  Author = {Vaughan, Timothy G and Drummond, Alexei J},  Date-Added = {2013-08-07 22:48:44 +0000},  Date-Modified = {2014-07-04 02:00:10 +0000},  Doi = {10.1093/molbev/mst057},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Keywords = {chemical kinetics simulation; epidemic modeling; phylogenetic trees; population genetics; stochastic simulation},  Month = {6},  Number = {6},  Pages = {1480-93},  Pmc = {PMC3649681},  Pmid = {23505043},  Pst = {ppublish},  Title = {A stochastic simulator of birth-death master equations with application to phylodynamics},  Volume = {30},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/mst057}}  @article{Gray:2011fk,  Abstract = {Staphylococcus aureus is a common cause of infections that has undergone rapid global spread over recent decades. Formal phylogeographic methods have not yet been applied to the molecular epidemiology of bacterial pathogens because the limited genetic diversity of data sets based on individual genes usually results in poor phylogenetic resolution. Here, we investigated a whole-genome single nucleotide polymorphism (SNP) data set of health care-associated Methicillin-resistant S. aureus sequence type 239 (HA-MRSA ST239) strains, which we analyzed using Markov spatial models that incorporate geographical sampling distributions. The reconstructed timescale indicated a temporal origin of this strain shortly after the introduction of Methicillin, followed by global pandemic spread. The estimate of the temporal origin was robust to the molecular clock, coalescent prior, full/intergenic/synonymous SNP inclusion, and correction for excluded invariant site patterns. Finally, phylogeographic analyses statistically supported the role of human movement in the global dissemination of HA-MRSA ST239, although it was unable to conclusively resolve the location of the root. This study demonstrates that bacterial genomes can indeed contain sufficient evolutionary information to elucidate the temporal and spatial dynamics of transmission. Future applications of this approach to other bacterial strains may provide valuable epidemiological insights that may justify the cost of genome-wide typing.},  Author = {Gray, Rebecca R and Tatem, Andrew J and others},  Date-Added = {2013-08-07 21:12:37 +0000},  Date-Modified = {2013-08-07 21:12:37 +0000},  Doi = {10.1093/molbev/msq319},  Fullauthor = {Gray, Rebecca R and Tatem, Andrew J and Johnson, Judith A and Alekseyenko, Alexander V and Pybus, Oliver G and Suchard, Marc A and Salemi, Marco},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Bayes Theorem; Communicable Diseases; Evolution, Molecular; Genome-Wide Association Study; Humans; Likelihood Functions; Markov Chains; Methicillin-Resistant Staphylococcus aureus; Models, Genetic; Phylogeny; Phylogeography; Staphylococcal Infections},  Month = {May},  Number = {5},  Pages = {1593-603},  Pmc = {PMC3115679},  Pmid = {21112962},  Pst = {ppublish},  Title = {Testing spatiotemporal hypothesis of bacterial evolution using methicillin-resistant Staphylococcus aureus ST239 genome-wide data within a bayesian framework},  Volume = {28},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msq319}}  @article{Rasmussen:2011qa,  Abstract = {Phylodynamics - the field aiming to quantitatively integrate the ecological and evolutionary dynamics of rapidly evolving populations like those of RNA viruses - increasingly relies upon coalescent approaches to infer past population dynamics from reconstructed genealogies. As sequence data have become more abundant, these approaches are beginning to be used on populations undergoing rapid and rather complex dynamics. In such cases, the simple demographic models that current phylodynamic methods employ can be limiting. First, these models are not ideal for yielding biological insight into the processes that drive the dynamics of the populations of interest. Second, these models differ in form from mechanistic and often stochastic population dynamic models that are currently widely used when fitting models to time series data. As such, their use does not allow for both genealogical data and time series data to be considered in tandem when conducting inference. Here, we present a flexible statistical framework for phylodynamic inference that goes beyond these current limitations. The framework we present employs a recently developed method known as particle MCMC to fit stochastic, nonlinear mechanistic models for complex population dynamics to gene genealogies and time series data in a Bayesian framework. We demonstrate our approach using a nonlinear Susceptible-Infected-Recovered (SIR) model for the transmission dynamics of an infectious disease and show through simulations that it provides accurate estimates of past disease dynamics and key epidemiological parameters from genealogies with or without accompanying time series data.},  Author = {Rasmussen, David A and Ratmann, Oliver and Koelle, Katia},  Date-Added = {2013-08-07 21:10:53 +0000},  Date-Modified = {2013-08-07 21:10:53 +0000},  Doi = {10.1371/journal.pcbi.1002136},  Journal = {PLoS Comp Biol},  Journal-Full = {PLoS computational biology},  Mesh = {Algorithms; Bayes Theorem; Computational Biology; Disease Transmission, Infectious; Epidemics; Epidemiologic Methods; Models, Biological; Monte Carlo Method; Nonlinear Dynamics; Phylogeny; Population Dynamics; Prevalence; Stochastic Processes},  Month = {Aug},  Number = {8},  Pages = {e1002136},  Pmc = {PMC3161897},  Pmid = {21901082},  Pst = {ppublish},  Title = {Inference for nonlinear epidemiological models using genealogies and time series},  Volume = {7},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.1002136}}  @article{welch2011b,  Author = {Welch, David},  Date-Added = {2013-08-07 21:10:34 +0000},  Date-Modified = {2013-08-07 21:16:05 +0000},  Doi = {10.3390/v3060659},  Issn = {1999-4915},  Journal = {Viruses},  Number = {6},  Pages = {659--676},  Title = {Is Network Clustering Detectable in Transmission Trees?},  Url = {http://www.mdpi.com/1999-4915/3/6/659/},  Volume = {3},  Year = {2011},  Bdsk-Url-1 = {http://www.mdpi.com/1999-4915/3/6/659/},  Bdsk-Url-2 = {http://dx.doi.org/10.3390/v3060659}}  @article{volz2012,  Author = {Volz, E. M.},  Date-Added = {2013-08-07 21:09:55 +0000},  Date-Modified = {2014-07-06 06:04:45 +0000},  Journal = {Genetics},  Number = {1},  Pages = {187--201},  Publisher = {Genetics Soc America},  Title = {Complex population dynamics and the coalescent under neutrality},  Volume = {190},  Year = {2012}}  @article{Ronquist:2012dz,  Abstract = {Since its introduction in 2001, MrBayes has grown in popularity as a software package for Bayesian phylogenetic inference using Markov chain Monte Carlo (MCMC) methods. With this note, we announce the release of version 3.2, a major upgrade to the latest official release presented in 2003. The new version provides convergence diagnostics and allows multiple analyses to be run in parallel with convergence progress monitored on the fly. The introduction of new proposals and automatic optimization of tuning parameters has improved convergence for many problems. The new version also sports significantly faster likelihood calculations through streaming single-instruction-multiple-data extensions (SSE) and support of the BEAGLE library, allowing likelihood calculations to be delegated to graphics processing units (GPUs) on compatible hardware. Speedup factors range from around 2 with SSE code to more than 50 with BEAGLE for codon problems. Checkpointing across all models allows long runs to be completed even when an analysis is prematurely terminated. New models include relaxed clocks, dating, model averaging across time-reversible substitution models, and support for hard, negative, and partial (backbone) tree constraints. Inference of species trees from gene trees is supported by full incorporation of the Bayesian estimation of species trees (BEST) algorithms. Marginal model likelihoods for Bayes factor tests can be estimated accurately across the entire model space using the stepping stone method. The new version provides more output options than previously, including samples of ancestral states, site rates, site d(N)/d(S) rations, branch rates, and node dates. A wide range of statistics on tree parameters can also be output for visualization in FigTree and compatible software.},  Author = {Ronquist, Fredrik and Teslenko, Maxim and others},  Date-Added = {2013-08-07 21:09:16 +0000},  Date-Modified = {2013-08-07 21:09:16 +0000},  Doi = {10.1093/sysbio/sys029},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Month = {May},  Number = {3},  Pages = {539-42},  Pmc = {PMC3329765},  Pmid = {22357727},  Pst = {ppublish},  Title = {{MrBayes} 3.2: efficient {Bayesian} phylogenetic inference and model choice across a large model space},  Volume = {61},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/sys029}}  @article{Drummond:2012fv,  Abstract = {Computational evolutionary biology, statistical phylogenetics and coalescent-based population genetics are becoming increasingly central to the analysis and understanding of molecular sequence data. We present the Bayesian Evolutionary Analysis by Sampling Trees (BEAST) software package version 1.7, which implements a family of Markov chain Monte Carlo (MCMC) algorithms for Bayesian phylogenetic inference, divergence time dating, coalescent analysis, phylogeography and related molecular evolutionary analyses. This package includes an enhanced graphical user interface program called Bayesian Evolutionary Analysis Utility (BEAUti) that enables access to advanced models for molecular sequence and phenotypic trait evolution that were previously available to developers only. The package also provides new tools for visualizing and summarizing multispecies coalescent and phylogeographic analyses. BEAUti and BEAST 1.7 are open source under the GNU lesser general public license and available at http://beast-mcmc.googlecode.com and http://beast.bio.ed.ac.uk.},  Author = {Drummond, Alexei J. and Suchard, Marc A and Xie, Dong and Rambaut, Andrew},  Date-Added = {2013-08-07 21:08:20 +0000},  Date-Modified = {2013-08-07 21:17:13 +0000},  Doi = {10.1093/molbev/mss075},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Animals; Base Sequence; Bayes Theorem; Computational Biology; DNA, Mitochondrial; Finches; Molecular Sequence Data; Phenotype; Phylogeny; Software; User-Computer Interface},  Month = {Aug},  Number = {8},  Pages = {1969-73},  Pmc = {PMC3408070},  Pmid = {22367748},  Pst = {ppublish},  Title = {Bayesian phylogenetics with {BEAUti} and the {BEAST} 1.7},  Volume = {29},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/mss075}}  @article{Gill2013,  Abstract = {Effective population size is fundamental in population genetics and characterizes genetic diversity. To infer past population dynamics from molecular sequence data, coalescent-based models have been developed for Bayesian nonparametric estimation of effective population size over time. Among the most successful is a Gaussian Markov random field (GMRF) model for a single gene locus. Here, we present a generalization of the GMRF model that allows for the analysis of multilocus sequence data. Using simulated data, we demonstrate the improved performance of our method to recover true population trajectories and the time to the most recent common ancestor (TMRCA). We analyze a multilocus alignment of HIV-1 CRF02_AG gene sequences sampled from Cameroon. Our results are consistent with HIV prevalence data and uncover some aspects of the population history that go undetected in Bayesian parametric estimation. Finally, we recover an older and more reconcilable TMRCA for a classic ancient DNA data set.},  Author = {Gill, Mandev S and Lemey, Philippe and Faria, Nuno R and Rambaut, Andrew and Shapiro, Beth and Suchard, Marc A},  Date-Added = {2013-05-14 22:08:31 +0000},  Date-Modified = {2014-07-04 01:54:06 +0000},  Doi = {10.1093/molbev/mss265},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Month = {3},  Number = {3},  Pages = {713-24},  Pmc = {PMC3563973},  Pmid = {23180580},  Pst = {ppublish},  Title = {Improving Bayesian population dynamics inference: a coalescent-based model for multiple loci},  Volume = {30},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/mss265}}  @article{HudsonKaplan1985,  Abstract = {Some statistical properties of samples of DNA sequences are studied under an infinite-site neutral model with recombination. The two quantities of interest are R, the number of recombination events in the history of a sample of sequences, and RM, the number of recombination events that can be parsimoniously inferred from a sample of sequences. Formulas are derived for the mean and variance of R. In contrast to R, RM can be determined from the sample. Since no formulas are known for the mean and variance of RM, they are estimated with Monte Carlo simulations. It is found that RM is often much less than R, therefore, the number of recombination events may be greatly under-estimated in a parsimonious reconstruction of the history of a sample. The statistic RM can be used to estimate the product of the recombination rate and the population size or, if the recombination rate is known, to estimate the population size. To illustrate this, DNA sequences from the Adh region of Drosophila melanogaster are used to estimate the effective population size of this species.},  Author = {Hudson, R R and Kaplan, N L},  Date-Added = {2013-05-14 00:23:43 +0000},  Date-Modified = {2014-07-04 02:01:26 +0000},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Alleles; Base Sequence; DNA; Mathematics; Models, Genetic; Recombination, Genetic},  Month = {9},  Number = {1},  Pages = {147-64},  Pmc = {PMC1202594},  Pmid = {4029609},  Pst = {ppublish},  Title = {Statistical properties of the number of recombination events in the history of a sample of DNA sequences},  Volume = {111},  Year = {1985}}  @article{Hudson1987,  Author = {Hudson, R R},  Date-Added = {2013-05-14 00:22:21 +0000},  Date-Modified = {2014-07-04 01:54:41 +0000},  Journal = {Genet Res},  Journal-Full = {Genetical research},  Mesh = {Animals; Genetic Linkage; Humans; Mathematics; Models, Genetic; Recombination, Genetic; Selection, Genetic},  Month = {12},  Number = {3},  Pages = {245-50},  Pmid = {3443297},  Pst = {ppublish},  Title = {Estimating the recombination parameter of a finite population model without selection},  Volume = {50},  Year = {1987}}  @article{Slatkin1991,  Abstract = {This paper describes the relationship between probabilities of identity by descent and the distribution of coalescence times. By using the relationship between coalescence times and identity probabilities, it is possible to extend existing results for inbreeding coefficients in regular systems of mating to find the distribution of coalescence times and the mean coalescence times. It is also possible to express Sewall Wright's FST as the ratio of average coalescence times of different pairs of genes. That simplifies the analysis of models of subdivided populations because the average coalescence time can be found by computing separately the time it takes for two genes to enter a single subpopulation and time it takes for two genes in the same subpopulation to coalesce. The first time depends only on the migration matrix and the second time depends only on the total number of individuals in the population. This approach is used to find FST in the finite island model and in one- and two-dimensional stepping-stone models. It is also used to find the rate of approach of FST to its equilibrium value. These results are discussed in terms of different measures of genetic distance. It is proposed that, for the purposes of describing the amount of gene flow among local populations, the effective migration rate between pairs of local populations, M, which is the migration rate that would be estimated for those two populations if they were actually in an island model, provides a simple and useful measure of genetic similarity that can be defined for either allozyme or DNA sequence data.},  Author = {Slatkin, M},  Date-Added = {2013-05-14 00:18:46 +0000},  Date-Modified = {2014-07-04 01:58:34 +0000},  Journal = {Genet Res},  Journal-Full = {Genetical research},  Mesh = {Animals; Genetics, Population; Inbreeding; Mathematics; Models, Genetic},  Month = {10},  Number = {2},  Pages = {167-75},  Pmid = {1765264},  Pst = {ppublish},  Title = {Inbreeding coefficients and coalescence times},  Volume = {58},  Year = {1991}}  @article{Takahata1989,  Abstract = {A genealogical relationship among genes at a locus (gene tree) sampled from three related populations was examined with special reference to population relatedness (population tree). A phylogenetically informative event in a gene tree constructed from nucleotide differences consists of interspecific coalescences of genes in each of which two genes sampled from different populations are descended from a common ancestor. The consistency probability between gene and population trees in which they are topologically identical was formulated in terms of interspecific coalescences. It was found that the consistency probability thus derived substantially increases as the sample size of genes increases, unless the divergence time of populations is very long compared to population sizes. Hence, there are cases where large samples at a locus are very useful in inferring a population tree.},  Author = {Takahata, N},  Date-Added = {2013-05-14 00:17:52 +0000},  Date-Modified = {2014-07-04 02:00:00 +0000},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Diploidy; Gene Frequency; Genes; Genetics, Population; Mathematics; Models, Genetic; Pedigree; Probability},  Month = {8},  Number = {4},  Pages = {957-66},  Pmc = {PMC1203770},  Pmid = {2759432},  Pst = {ppublish},  Title = {Gene genealogy in three related populations: consistency probability between gene and population trees},  Volume = {122},  Year = {1989}}  @article{Tajima1989,  Abstract = {Using the two subpopulation model, the expected numbers of segregating sites in a number of DNA sequences randomly sampled from a subdivided population were examined for several types of population subdivisions. It is shown that, in the case where the pattern of migration is symmetrical such as the finite island model, the expected number of segregating sites is independent of the migration rate when two or three DNA sequences are randomly sampled from the same subpopulation, but depends on the migration rate when more than three DNA sequences are sampled. It is also shown that the population subdivision can increase the amount of DNA polymorphism even in a subpopulation in some cases.},  Author = {Tajima, F},  Date-Added = {2013-05-14 00:16:58 +0000},  Date-Modified = {2014-07-04 01:59:47 +0000},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {DNA; Genetics, Population; Models, Genetic; Polymorphism, Genetic},  Month = {9},  Number = {1},  Pages = {229-40},  Pmc = {PMC1203786},  Pmid = {2806885},  Pst = {ppublish},  Title = {DNA polymorphism in a subdivided population: the expected number of segregating sites in the two-subpopulation model},  Volume = {123},  Year = {1989}}  @article{Tajima1983,  Abstract = {With the aim of analyzing and interpreting data on DNA polymorphism obtained by DNA sequencing or restriction enzyme technique, a mathematical theory on the expected evolutionary relationship among DNA sequences (nucleons) sampled is developed under the assumption that the evolutionary change of nucleons is determined solely by mutation and random genetic drift. The statistical property of the number of nucleotide differences between randomly chosen nucleons and that of heterozygosity or nucleon diversity is investigated using this theory. These studies indicate that the estimates of the average number of nucleotide differences and nucleon diversity have a large variance, and a large part of this variance is due to stochastic factors. Therefore, increasing sample size does not help reduce the variance significantly The distribution of sample allele (nucleomorph) frequencies is also studied, and it is shown that a small number of samples are sufficient in order to know the distribution pattern.},  Author = {Tajima, F},  Date-Added = {2013-05-14 00:15:50 +0000},  Date-Modified = {2014-07-04 01:59:35 +0000},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Base Sequence; Biological Evolution; DNA; Genetics, Population; Models, Genetic; Polymorphism, Genetic},  Month = {10},  Number = {2},  Pages = {437-60},  Pmc = {PMC1202167},  Pmid = {6628982},  Pst = {ppublish},  Title = {Evolutionary relationship of DNA sequences in finite populations},  Volume = {105},  Year = {1983}}  @article{Lartillot_etal2009,  Abstract = {MOTIVATION: A variety of probabilistic models describing the evolution of DNA or protein sequences have been proposed for phylogenetic reconstruction or for molecular dating. However, there still lacks a common implementation allowing one to freely combine these independent features, so as to test their ability to jointly improve phylogenetic and dating accuracy. RESULTS: We propose a software package, PhyloBayes 3, which can be used for conducting Bayesian phylogenetic reconstruction and molecular dating analyses, using a large variety of amino acid replacement and nucleotide substitution models, including empirical mixtures or non-parametric models, as well as alternative clock relaxation processes.},  Author = {Lartillot, Nicolas and Lepage, Thomas and Blanquart, Samuel},  Date-Added = {2013-05-10 09:12:12 +1200},  Date-Modified = {2014-07-04 01:55:18 +0000},  Doi = {10.1093/bioinformatics/btp368},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Mesh = {Animals; Bayes Theorem; Computational Biology; Databases, Nucleic Acid; Phylogeny; Predictive Value of Tests; Reproducibility of Results; Software; Time Factors},  Month = {9},  Number = {17},  Pages = {2286-8},  Pmid = {19535536},  Pst = {ppublish},  Title = {PhyloBayes 3: a Bayesian software package for phylogenetic reconstruction and molecular dating},  Volume = {25},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/btp368}}  @article{PagelMeade2004,  Author = {Pagel, Mark D. and Meade, Andrew},  Date-Added = {2013-05-10 09:08:58 +1200},  Date-Modified = {2014-07-06 06:03:51 +0000},  Doi = {10.1080/10635150490468675},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Mesh = {Base Sequence; Codon; Computer Simulation; Genes; Likelihood Functions; Markov Chains; Models, Biological; Models, Genetic; Monte Carlo Method; Pattern Recognition, Automated; Phylogeny; RNA, Ribosomal},  Month = {Aug},  Number = {4},  Pages = {571-81},  Pmid = {15371247},  Pst = {ppublish},  Title = {A phylogenetic mixture model for detecting pattern-heterogeneity in gene sequence or character-state data},  Volume = {53},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1080/10635150490468675}}  @article{WilsonBalding1998,  Abstract = {Ease and accuracy of typing, together with high levels of polymorphism and widespread distribution in the genome, make microsatellite (or short tandem repeat) loci an attractive potential source of information about both population histories and evolutionary processes. However, microsatellite data are difficult to interpret, in particular because of the frequency of back-mutations. Stochastic models for the underlying genetic processes can be specified, but in the past they have been too complicated for direct analysis. Recent developments in stochastic simulation methodology now allow direct inference about both historical events, such as genealogical coalescence times, and evolutionary parameters, such as mutation rates. A feature of the Markov chain Monte Carlo (MCMC) algorithm that we propose here is that the likelihood computations are simplified by treating the (unknown) ancestral allelic states as auxiliary parameters. We illustrate the algorithm by analyzing microsatellite samples simulated under the model. Our results suggest that a single microsatellite usually does not provide enough information for useful inferences, but that several completely linked microsatellites can be informative about some aspects of genealogical history and evolutionary processes. We also reanalyze data from a previously published human Y chromosome microsatellite study, finding evidence for an effective population size for human Y chromosomes in the low thousands and a recent time since their most recent common ancestor: the 95% interval runs from approximately 15, 000 to 130,000 years, with most likely values around 30,000 years.},  Author = {Wilson, I J and Balding, D J},  Date-Added = {2013-05-10 08:57:52 +1200},  Date-Modified = {2013-05-10 08:58:27 +1200},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Genetics, Population; Humans; Microsatellite Repeats; Models, Genetic; Mutation; Pedigree; Y Chromosome},  Month = {Sep},  Number = {1},  Pages = {499-510},  Pmc = {PMC1460328},  Pmid = {9725864},  Pst = {ppublish},  Title = {Genealogical inference from microsatellite data},  Volume = {150},  Year = {1998}}  @article{Drummond2002,  Abstract = {Molecular sequences obtained at different sampling times from populations of rapidly evolving pathogens and from ancient subfossil and fossil sources are increasingly available with modern sequencing technology. Here, we present a Bayesian statistical inference approach to the joint estimation of mutation rate and population size that incorporates the uncertainty in the genealogy of such temporally spaced sequences by using Markov chain Monte Carlo (MCMC) integration. The Kingman coalescent model is used to describe the time structure of the ancestral tree. We recover information about the unknown true ancestral coalescent tree, population size, and the overall mutation rate from temporally spaced data, that is, from nucleotide sequences gathered at different times, from different individuals, in an evolving haploid population. We briefly discuss the methodological implications and show what can be inferred, in various practically relevant states of prior knowledge. We develop extensions for exponentially growing population size and joint estimation of substitution model parameters. We illustrate some of the important features of this approach on a genealogy of HIV-1 envelope (env) partial sequences.},  Author = {Drummond, Alexei J and Nicholls, Geoff K and Rodrigo, Allen G and Solomon, Wiremu},  Date-Added = {2013-05-09 22:20:09 +1200},  Date-Modified = {2014-07-04 01:53:36 +0000},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Decision Trees; Genealogy and Heraldry; Genetics, Population; Markov Chains; Models, Genetic; Monte Carlo Method; Mutation; Time},  Month = {7},  Number = {3},  Pages = {1307-20},  Pmc = {PMC1462188},  Pmid = {12136032},  Pst = {ppublish},  Title = {Estimating mutation parameters, population history and genealogy simultaneously from temporally spaced sequence data},  Volume = {161},  Year = {2002}}  @phdthesis{Li1996,  Author = {Li, S.},  Date-Added = {2013-05-09 22:08:01 +1200},  Date-Modified = {2013-05-09 22:09:00 +1200},  School = {Ohio State University, Columbus},  Title = {Phylogenetic tree construction using Markov chain Monte Carlo.},  Year = {1996}}  @article{Kuhner:2006uq,  Abstract = {We present a Markov chain Monte Carlo coalescent genealogy sampler, LAMARC 2.0, which estimates population genetic parameters from genetic data. LAMARC can co-estimate subpopulation Theta = 4N(e)mu, immigration rates, subpopulation exponential growth rates and overall recombination rate, or a user-specified subset of these parameters. It can perform either maximum-likelihood or Bayesian analysis, and accomodates nucleotide sequence, SNP, microsatellite or elecrophoretic data, with resolved or unresolved haplotypes. It is available as portable source code and executables for all three major platforms. AVAILABILITY: LAMARC 2.0 is freely available at http://evolution.gs.washington.edu/lamarc},  Author = {Kuhner, Mary K},  Date-Added = {2013-05-06 22:23:18 +1200},  Date-Modified = {2013-05-06 22:23:18 +1200},  Doi = {10.1093/bioinformatics/btk051},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Mesh = {Bayes Theorem; Biological Evolution; Chromosome Mapping; Computer Simulation; DNA Mutational Analysis; Genetic Variation; Genetics, Population; Likelihood Functions; Models, Genetic; Models, Statistical; Software},  Month = {Mar},  Number = {6},  Pages = {768-70},  Pmid = {16410317},  Pst = {ppublish},  Title = {LAMARC 2.0: maximum likelihood and Bayesian estimation of population parameters},  Volume = {22},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/btk051}}  @article{Pamilo:1988fk,  Abstract = {It is well known that a phylogenetic tree (gene tree) constructed from DNA sequences for a genetic locus does not necessarily agree with the tree that represents the actual evolutionary pathway of the species involved (species tree). One of the important factors that cause this difference is genetic polymorphism in the ancestral species. Under the assumption of neutral mutations, this problem can be studied by evaluating the probability (P) that a gene tree has the same topology as that of the species tree. When one gene (allele) is used from each of the species involved, the probability can be expressed as a simple function of Ti = ti/(2N), where ti is the evolutionary time measured in generations for the ith internodal branch of the species tree and N is the effective population size. When any of the Ti's is less than 1, the probability P becomes considerably less than 1.0. This probability cannot be substantially increased by increasing the number of alleles sampled from a locus. To increase the probability, one has to use DNA sequences from many different loci that have evolved independently of each other.},  Author = {Pamilo, P and Nei, M},  Date-Added = {2013-05-06 00:24:00 +0000},  Date-Modified = {2014-07-04 01:55:56 +0000},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Alleles; Animals; Biological Evolution; DNA; Humans; Models, Genetic; Phylogeny; Polymorphism, Genetic; Probability},  Month = {9},  Number = {5},  Pages = {568-83},  Pmid = {3193878},  Pst = {ppublish},  Title = {Relationships between gene trees and species trees},  Volume = {5},  Year = {1988}}  @article{Volz:2013fk,  Abstract = {Viral phylodynamics is defined as the study of how epidemiological, immunological, and evolutionary processes act and potentially interact to shape viralphylogenies. Since the coining of the term in 2004, research on viral phylodynamics has focused on transmission dynamics in an effort to shed light on how these dynamics impact viral genetic variation. Transmission dynamics can be considered at the level of cells within an infected host, individual hosts within a population, or entire populations of hosts. Many viruses, especially RNA viruses, rapidly accumulate genetic variation because of short generation times and high mutation rates. Patterns of viral genetic variation are therefore heavily influenced by how quickly transmission occurs and by which entities transmit to one another. Patterns of viral genetic variation will also be affected by selection acting on viral phenotypes. Although viruses can differ with respect to many phenotypes, phylodynamic studies have to date tended to focus on a limited number of viral phenotypes. These include virulence phenotypes, phenotypes associated with viral transmissibility, cell or tissue tropism phenotypes, and antigenic phenotypes that can facilitate escape from host immunity. Due to the impact that transmission dynamics and selection can have on viral genetic variation, viral phylogenies can therefore be used to investigate important epidemiological, immunological, and evolutionary processes, such as epidemic spread[2], spatio-temporal dynamics including metapopulation dynamics[3], zoonotic transmission, tissue tropism[4], and antigenic drift[5]. The quantitative investigation of these processes through the consideration of viral phylogenies is the central aim of viral phylodynamics.},  Author = {Volz, Erik M and Koelle, Katia and Bedford, Trevor},  Date-Added = {2013-05-05 23:13:58 +1200},  Date-Modified = {2013-05-05 23:13:58 +1200},  Doi = {10.1371/journal.pcbi.1002947},  Journal = {PLoS Comput Biol},  Journal-Full = {PLoS computational biology},  Month = {Mar},  Number = {3},  Pages = {e1002947},  Pmc = {PMC3605911},  Pmid = {23555203},  Pst = {ppublish},  Title = {Viral phylodynamics},  Volume = {9},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.1002947}}  @article{Jeffreys1946,  Author = {Jeffreys, H.},  Date-Added = {2013-04-28 21:32:39 +1200},  Date-Modified = {2013-04-28 21:33:27 +1200},  Journal = {Proceedings of the Royal Society of London. Series A. Mathematical and Physical Sciences},  Number = {1007},  Pages = {453--461},  Title = {An invariant form for the prior probability in estimation problems},  Volume = {186},  Year = {1946}}  @book{Laplace1812,  Author = {Laplace, P.},  Date-Added = {2013-04-28 21:00:48 +1200},  Date-Modified = {2013-04-28 21:01:54 +1200},  Publisher = {Courcier, Paris},  Title = {Theorie Analytique des Probabilites},  Year = {1812}}  @article{Pereira:2009uq,  Abstract = {We analyzed the current status (as of the end of August 2008) of human mitochondrial genomes deposited in GenBank, amounting to 5140 complete or coding-region sequences, in order to present an overall picture of the diversity present in the mitochondrial DNA of the global human population. To perform this task, we developed mtDNA-GeneSyn, a computer tool that identifies and exhaustedly classifies the diversity present in large genetic data sets. The diversity observed in the 5140 human mitochondrial genomes was compared with all possible transitions and transversions from the standard human mitochondrial reference genome. This comparison showed that tRNA and rRNA secondary structures have a large effect in limiting the diversity of the human mitochondrial sequences, whereas for the protein-coding genes there is a bias toward less variation at the second codon positions. The analysis of the observed amino acid variations showed a tolerance of variations that convert between the amino acids V, I, A, M, and T. This defines a group of amino acids with similar chemical properties that can interconvert by a single transition.},  Author = {Pereira, Lu{\'\i}sa and Freitas, Fernando and Fernandes, Ver{\'o}nica and Pereira, Joana B and Costa, Marta D and Costa, Stephanie and M{\'a}ximo, Valdemar and Macaulay, Vincent and Rocha, Ricardo and Samuels, David C},  Date-Added = {2013-04-28 11:35:39 +1200},  Date-Modified = {2013-04-28 11:35:39 +1200},  Doi = {10.1016/j.ajhg.2009.04.013},  Journal = {Am J Hum Genet},  Journal-Full = {American journal of human genetics},  Mesh = {Base Sequence; DNA, Mitochondrial; Databases, Genetic; Genetic Variation; Genome, Human; Genome, Mitochondrial; Humans; Molecular Sequence Data; Nucleic Acid Conformation; RNA, Transfer},  Month = {May},  Number = {5},  Pages = {628-40},  Pmc = {PMC2681004},  Pmid = {19426953},  Pst = {ppublish},  Title = {The diversity present in 5140 human mitochondrial genomes},  Volume = {84},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ajhg.2009.04.013}}  @article{Redelings:2007fk,  Abstract = {BACKGROUND: Phylogenies of rapidly evolving pathogens can be difficult to resolve because of the small number of substitutions that accumulate in the short times since divergence. To improve resolution of such phylogenies we propose using insertion and deletion (indel) information in addition to substitution information. We accomplish this through joint estimation of alignment and phylogeny in a Bayesian framework, drawing inference using Markov chain Monte Carlo. Joint estimation of alignment and phylogeny sidesteps biases that stem from conditioning on a single alignment by taking into account the ensemble of near-optimal alignments.  RESULTS: We introduce a novel Markov chain transition kernel that improves computational efficiency by proposing non-local topology rearrangements and by block sampling alignment and topology parameters. In addition, we extend our previous indel model to increase biological realism by placing indels preferentially on longer branches. We demonstrate the ability of indel information to increase phylogenetic resolution in examples drawn from within-host viral sequence samples. We also demonstrate the importance of taking alignment uncertainty into account when using such information. Finally, we show that codon-based substitution models can significantly affect alignment quality and phylogenetic inference by unrealistically forcing indels to begin and end between codons.  CONCLUSION: These results indicate that indel information can improve phylogenetic resolution of recently diverged pathogens and that alignment uncertainty should be considered in such analyses.},  Author = {Redelings, Benjamin D and Suchard, Marc A},  Date-Added = {2013-04-28 10:06:01 +1200},  Date-Modified = {2013-04-28 10:06:01 +1200},  Doi = {10.1186/1471-2148-7-40},  Journal = {BMC Evol Biol},  Journal-Full = {BMC evolutionary biology},  Mesh = {Base Sequence; Bayes Theorem; Codon, Terminator; Frameshift Mutation; Genes, Viral; HIV-1; Markov Chains; Models, Genetic; Phylogeny; Sequence Alignment; Simian immunodeficiency virus},  Pages = {40},  Pmc = {PMC1853084},  Pmid = {17359539},  Pst = {epublish},  Title = {Incorporating indel information into phylogeny estimation for rapidly emerging pathogens},  Volume = {7},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2148-7-40}}  @article{Bofkin:2007vn,  Author = {Bofkin, Lee and Goldman, Nick},  Date-Added = {2013-04-25 12:40:22 +1200},  Date-Modified = {2014-07-05 08:51:35 +0000},  Doi = {10.1093/molbev/msl178},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Base Sequence; Codon; Computational Biology; Databases, Nucleic Acid; Evolution, Molecular; Models, Genetic; Models, Statistical; Proteins; Sequence Alignment},  Month = {Feb},  Number = {2},  Pages = {513-21},  Pmid = {17119011},  Pst = {ppublish},  Title = {Variation in evolutionary processes at different codon positions},  Volume = {24},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msl178}}  @article{Sullivan1999effect,  Author = {Sullivan, Jack and Swofford, David L and Naylor, Gavin JP},  Date-Added = {2013-04-25 10:55:54 +1200},  Date-Modified = {2013-04-25 10:56:50 +1200},  Journal = {Molecular Biology and Evolution},  Pages = {1347--1356},  Title = {The effect of taxon sampling on estimating rate heterogeneity parameters of maximum-likelihood models},  Volume = {16},  Year = {1999}}  @incollection{WaddellPenny1996,  Author = {Waddell, P. and Penny, D.},  Booktitle = {Handbook of symbolic evolution},  Date-Added = {2013-04-25 10:47:21 +1200},  Date-Modified = {2013-08-10 08:18:28 +0000},  Editor = {Lock, A. J. and Peters, C. R.},  Pages = {53--73},  Publisher = {Clarendon Press, Oxford.},  Title = {Evolutionary trees of apes and humans from {DNA} sequences},  Year = {1996}}  @article{Gu:1995kx,  Abstract = {This paper presents a maximum likelihood approach to estimating the variation of substitution rate among nucleotide sites. We assume that the rate varies among sites according to an invariant+gamma distribution, which has two parameters: the gamma parameter alpha and the proportion of invariable sites theta. Theoretical treatments on three, four, and five sequences have been conducted, and computer program have been developed. It is shown that rho = (1 + theta alpha)/(1 + alpha) is a good measure for the rate heterogeneity among sites. Extensive simulations show that (1) if the proportion of invariable sites is negligible, i.e., theta = 0, the gamma parameter alpha can be satisfactorily estimated, even with three sequences; (2) if the proportion of invariable sites is not negligible, the heterogeneity rho can still be suitably estimated with four or more sequences; and (3) the distances estimated by the proposed method are almost unbiased and are robust against violation of the assumption of the invariant + gamma distribution.},  Author = {Gu, X and Fu, Y X and Li, W H},  Date-Added = {2013-04-25 10:45:54 +1200},  Date-Modified = {2013-04-25 10:45:54 +1200},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Computer Simulation; DNA; Genetic Variation; Likelihood Functions; Models, Genetic; Nucleotides; RNA, Ribosomal},  Month = {Jul},  Number = {4},  Pages = {546-57},  Pmid = {7659011},  Pst = {ppublish},  Title = {Maximum likelihood estimation of the heterogeneity of substitution rate among nucleotide sites},  Volume = {12},  Year = {1995}}  @article{Nee:2001uq,  Abstract = {It is possible to estimate the rate of diversification of clades from phylogenies with a temporal dimension. First, I present several methods for constructing confidence intervals for the speciation rate under the simple assumption of a pure birth process. I discuss the relationships among these methods in the hope of clarifying some fundamental theory in this area. Their performances are compared in a simulation study and one is recommended for use as a result. A variety of other questions that may, in fact, be the questions of primary interest (e.g., Has the rate of cladogenesis been declining?) are then recast as biological variants of the purely statistical question-Is the birth process model appropriate for my data? Seen in this way, a preexisting arsenal of statistical techniques is opened up for use in this area: in particular, techniques developed for the analysis of Poisson processes and the analysis of survival data. These two approaches start from different representations of the data--the branch lengths in the tree--and I explicitly relate the two. Aiming for a synoptic account of useful theory in this area, I briefly discuss some important results from the analysis of two distinct birth-death processes: the one introduced into this area by Hey (1992) is refitted with some powerful statistical tools.},  Author = {Nee, S. C.},  Date-Added = {2013-04-24 17:20:53 +1200},  Date-Modified = {2014-07-06 00:58:34 +0000},  Journal = {Evolution},  Journal-Full = {Evolution; international journal of organic evolution},  Mesh = {Animals; Biological Evolution; Computer Simulation; Confidence Intervals; Genetic Variation; Likelihood Functions; Models, Genetic; Phylogeny; Species Specificity},  Month = {Apr},  Number = {4},  Pages = {661-8},  Pmid = {11392383},  Pst = {ppublish},  Title = {Inferring speciation rates from phylogenies},  Volume = {55},  Year = {2001}}  @article{Nee:1994fk,  Abstract = {Molecular phylogenies can be used to reject null models of the way we think evolution occurred, including patterns of lineage extinction. They can also be used to provide maximum likelihood estimates of parameters associated with lineage birth and death rates. We illustrate: (i) how molecular phylogenies provide information about the extent to which particular clades are likely to be under threat from extinction; (ii) how cursory analyses of molecular phylogenies can lead to incorrect conclusions about the evolutionary processes that have been at work; and (iii) how different evolutionary processes leave distinctive marks on the structure of reconstructed phylogenies.},  Author = {Nee, S. C. and Holmes, E. C. and May, R. M. and Harvey, P. H.},  Date-Added = {2013-04-24 17:19:39 +1200},  Date-Modified = {2014-07-07 01:20:50 +0000},  Doi = {10.1098/rstb.1994.0054},  Journal = {Philos Trans R Soc Lond B Biol Sci},  Journal-Full = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},  Mesh = {Animals; Birth Rate; Drosophila; HIV-1; Molecular Biology; Mortality; Phylogeny; Urodela},  Month = {Apr},  Number = {1307},  Pages = {77-82},  Pmid = {8878259},  Pst = {ppublish},  Title = {Extinction rates can be estimated from molecular phylogenies},  Volume = {344},  Year = {1994},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rstb.1994.0054}}  @article{Cann:1987kx,  Abstract = {Mitochondrial DNAs from 147 people, drawn from five geographic populations have been analysed by restriction mapping. All these mitochondrial DNAs stem from one woman who is postulated to have lived about 200,000 years ago, probably in Africa. All the populations examined except the African population have multiple origins, implying that each area was colonised repeatedly.},  Author = {Cann, R L and Stoneking, M and Wilson, A C},  Date = {1987 Jan 1-7},  Date-Added = {2013-02-15 23:46:12 +1300},  Date-Modified = {2013-02-15 23:46:12 +1300},  Doi = {10.1038/325031a0},  Journal = {Nature},  Journal-Full = {Nature},  Mesh = {Biological Evolution; Chromosome Mapping; DNA; DNA Restriction Enzymes; DNA, Mitochondrial; Female; Humans; Male; Mathematics},  Number = {6099},  Pages = {31-6},  Pmid = {3025745},  Pst = {ppublish},  Title = {Mitochondrial DNA and human evolution},  Volume = {325},  Year = {1987},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/325031a0}}  @article{Vigilant:1991uq,  Abstract = {The proposal that all mitochondrial DNA (mtDNA) types in contemporary humans stem from a common ancestor present in an African population some 200,000 years ago has attracted much attention. To study this proposal further, two hypervariable segments of mtDNA were sequenced from 189 people of diverse geographic origin, including 121 native Africans. Geographic specificity was observed in that identical mtDNA types are shared within but not between populations. A tree relating these mtDNA sequences to one another and to a chimpanzee sequence has many deep branches leading exclusively to African mtDNAs. An African origin for human mtDNA is supported by two statistical tests. With the use of the chimpanzee and human sequences to calibrate the rate of mtDNA evolution, the age of the common human mtDNA ancestor is placed between 166,000 and 249,000 years. These results thus support and extend the African origin hypothesis of human mtDNA evolution.},  Author = {Vigilant, L and Stoneking, M and Harpending, H and Hawkes, K and Wilson, A C},  Date-Added = {2013-02-15 23:33:31 +1300},  Date-Modified = {2013-02-15 23:33:31 +1300},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Africa; African Continental Ancestry Group; Animals; Biological Evolution; DNA, Mitochondrial; Genome, Human; Haplorhini; Humans; Models, Genetic; Restriction Mapping},  Month = {Sep},  Number = {5027},  Pages = {1503-7},  Pmid = {1840702},  Pst = {ppublish},  Title = {African populations and the evolution of human mitochondrial DNA},  Volume = {253},  Year = {1991}}  @article{WilsonSarich1969,  Abstract = {We discuss published molecular evidence concerning the relationship of man to African apes and Old World monkeys. Quantitative comparisons of their serum albumins, transferrins, hemoglobins, and DNA show that man is genetically much more similar to the African apes than to the Old World monkeys. The amino acid sequences of hemoglobins from humans, chimpanzees, gorillas, and rhesus monkeys are consistent with the hypothesis that the probability of an amino acid substitution occurring in a given interval of time is the same for every hemoglobin lineage. This allows the use of these data as a hemoglobin evolutionary clock, just as we have previously done with the albumins. It is shown that concordance exists between the hemoglobin and albumin results and that both support the suggestion that the human lineage diverged from that leading to the African apes far more recently than is generally supposed. Considering both the albumin and hemoglobin data, we would set the most probable date at 4 to 5 million years.},  Author = {Wilson, A C and Sarich, V M},  Date-Added = {2013-02-15 23:16:13 +1300},  Date-Modified = {2015-09-03 14:19:41 +0000},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Amino Acid Sequence; Animals; Biological Evolution; Blood Proteins; DNA; Haplorhini; Hemoglobins; Hominidae; Humans; Models, Biological; Serum Albumin; Transferrin},  Month = {Aug},  Number = {4},  Pages = {1088-93},  Pmc = {PMC223432},  Pmid = {4982244},  Pst = {ppublish},  Title = {A molecular time scale for human evolution},  Volume = {63},  Year = {1969}}  @inproceedings{PalaciosMinin2012,  Author = {Palacios, J. A. and Minin, V. N.},  Booktitle = {Proc. 28th Conf. on Uncertainty in Artificial Intelligence},  Date-Added = {2013-02-14 00:52:28 +0000},  Date-Modified = {2013-02-14 00:52:28 +0000},  Editor = {de Freitas, N. and Murphy, K.},  Pages = {726-735},  Publisher = {AUAI Press},  Title = {Integrated nested Laplace approximation for Bayesian nonparametric phylodynamics.},  Year = {2012}}  @article{PalaciosMinin2013,  Author = {Palacios, J. A. and Minin, V. N.},  Date-Added = {2013-02-14 00:52:28 +0000},  Date-Modified = {2013-02-14 00:52:28 +0000},  Journal = {Biometrics},  Title = {Gaussian process-based Bayesian nonparametric inference of population trajectories from gene genealogies},  Volume = {in press},  Year = {2013}}  @article{sashaCounting,  Author = {Gavryushkina, Alexandra and Welch, David and Drummond, Alexei J.},  Date-Added = {2013-02-13 20:36:25 +1300},  Date-Modified = {2014-07-05 10:32:50 +0000},  Journal = {Algorithms in Molecular Biology},  Title = {Recursive Algorithms for Phylogenetic Tree Counting},  Volume = {submitted},  Year = {2013}}  @article{Arunapuram:2013vn,  Abstract = {MOTIVATION: Comparative modeling of RNA is known to be important for making accurate secondary structure predictions. RNA structure prediction tools such as PPfold or RNAalifold use an aligned set of sequences in predictions. Obtaining a multiple alignment from a set of sequences is quite a challenging problem itself, and the quality of the alignment can affect the quality of a prediction. By implementing RNA secondary structure prediction in a statistical alignment framework, and predicting structures from multiple alignment samples instead of a single fixed alignment, it may be possible to improve predictions. RESULTS: We have extended the program StatAlign to make use of RNA-specific features, which include RNA secondary structure prediction from multiple alignments using either a thermodynamic approach (RNAalifold) or a Stochastic Context-Free Grammars (SCFGs) approach (PPfold). We also provide the user with scores relating to the quality of a secondary structure prediction, such as information entropy values for the combined space of secondary structures and sampled alignments, and a reliability score that predicts the expected number of correctly predicted base pairs. Finally, we have created RNA secondary structure visualization plugins and automated the process of setting up Markov Chain Monte Carlo runs for RNA alignments in StatAlign.Availability and implementation: The software is available from http://statalign.github.com/statalign/.Contact: [email protected] information: Supplementary data are available at Bioinformatics online.},  Author = {Arunapuram, Preeti and Edvardsson, Ingolfur and Golden, Michael and Anderson, James W J and Nov{\'a}k, Ad{\'a}m and S{\"u}k{\"o}sd, Zsuzsanna and Hein, Jotun},  Date-Added = {2013-02-13 03:50:20 +0000},  Date-Modified = {2013-02-13 03:50:20 +0000},  Doi = {10.1093/bioinformatics/btt025},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Month = {Feb},  Pmid = {23335014},  Pst = {aheadofprint},  Title = {StatAlign 2.0: combining statistical alignment with RNA secondary structure prediction},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/btt025}}  @article{Novak:2008kx,  Abstract = {MOTIVATION: Bayesian analysis is one of the most popular methods in phylogenetic inference. The most commonly used methods fix a single multiple alignment and consider only substitutions as phylogenetically informative mutations, though alignments and phylogenies should be inferred jointly as insertions and deletions also carry informative signals. Methods addressing these issues have been developed only recently and there has not been so far a user-friendly program with a graphical interface that implements these methods. RESULTS: We have developed an extendable software package in the Java programming language that samples from the joint posterior distribution of phylogenies, alignments and evolutionary parameters by applying the Markov chain Monte Carlo method. The package also offers tools for efficient on-the-fly summarization of the results. It has a graphical interface to configure, start and supervise the analysis, to track the status of the Markov chain and to save the results. The background model for insertions and deletions can be combined with any substitution model. It is easy to add new substitution models to the software package as plugins. The samples from the Markov chain can be summarized in several ways, and new postprocessing plugins may also be installed.},  Author = {Nov{\'a}k, Ad{\'a}m and Mikl{\'o}s, Istv{\'a}n and Lyngs{\o}, Rune and Hein, Jotun},  Date-Added = {2013-02-13 03:50:19 +0000},  Date-Modified = {2013-02-13 03:50:19 +0000},  Doi = {10.1093/bioinformatics/btn457},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Mesh = {Bayes Theorem; Evolution, Molecular; Markov Chains; Phylogeny; Sequence Alignment; Software},  Month = {Oct},  Number = {20},  Pages = {2403-4},  Pmid = {18753153},  Pst = {ppublish},  Title = {StatAlign: an extendable software package for joint Bayesian estimation of alignments and evolutionary trees},  Volume = {24},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/btn457}}  @article{Bradley:2009uq,  Abstract = {We describe a new program for the alignment of multiple biological sequences that is both statistically motivated and fast enough for problem sizes that arise in practice. Our Fast Statistical Alignment program is based on pair hidden Markov models which approximate an insertion/deletion process on a tree and uses a sequence annealing algorithm to combine the posterior probabilities estimated from these models into a multiple alignment. FSA uses its explicit statistical model to produce multiple alignments which are accompanied by estimates of the alignment accuracy and uncertainty for every column and character of the alignment--previously available only with alignment programs which use computationally-expensive Markov Chain Monte Carlo approaches--yet can align thousands of long sequences. Moreover, FSA utilizes an unsupervised query-specific learning procedure for parameter estimation which leads to improved accuracy on benchmark reference alignments in comparison to existing programs. The centroid alignment approach taken by FSA, in combination with its learning procedure, drastically reduces the amount of false-positive alignment on biological data in comparison to that given by other methods. The FSA program and a companion visualization tool for exploring uncertainty in alignments can be used via a web interface at http://orangutan.math.berkeley.edu/fsa/, and the source code is available at http://fsa.sourceforge.net/.},  Author = {Bradley, Robert K and Roberts, Adam and Smoot, Michael and Juvekar, Sudeep and Do, Jaeyoung and Dewey, Colin and Holmes, Ian and Pachter, Lior},  Date-Added = {2013-02-13 03:43:10 +0000},  Date-Modified = {2013-02-13 03:43:10 +0000},  Doi = {10.1371/journal.pcbi.1000392},  Journal = {PLoS Comput Biol},  Journal-Full = {PLoS computational biology},  Mesh = {Algorithms; Amino Acid Sequence; Animals; Artificial Intelligence; Base Sequence; Data Interpretation, Statistical; Databases, Genetic; Humans; Markov Chains; Models, Genetic; Molecular Sequence Data; Sensitivity and Specificity; Sequence Alignment; Sequence Analysis; Software},  Month = {May},  Number = {5},  Pages = {e1000392},  Pmc = {PMC2684580},  Pmid = {19478997},  Pst = {ppublish},  Title = {Fast statistical alignment},  Volume = {5},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.1000392}}  @phdthesis{drummond2002computational,  Author = {Drummond, Alexei J.},  Date-Added = {2013-02-13 01:57:28 +0000},  Date-Modified = {2013-02-13 02:00:21 +0000},  School = {University of Auckland},  Title = {Computational Statistical Inference for Molecular Evolution and Population Genetics},  Year = {2002}}  @article{Stadler:2013fk,  Abstract = {Host population structure has a major influence on epidemiological dynamics. However, in particular for sexually transmitted diseases, quantitative data on population contact structure are hard to obtain. Here, we introduce a new method that quantifies host population structure based on phylogenetic trees, which are obtained from pathogen genetic sequence data. Our method is based on a maximum-likelihood framework and uses a multi-type branching process, under which each host is assigned to a type (subpopulation). In a simulation study, we show that our method produces accurate parameter estimates for phylogenetic trees in which each tip is assigned to a type, as well for phylogenetic trees in which the type of the tip is unknown. We apply the method to a Latvian HIV-1 dataset, quantifying the impact of the intravenous drug user epidemic on the heterosexual epidemic (known tip states), and identifying superspreader dynamics within the men-having-sex-with-men epidemic (unknown tip states).},  Author = {Stadler, Tanja and Bonhoeffer, Sebastian},  Date-Added = {2013-02-13 01:53:53 +0000},  Date-Modified = {2013-02-13 01:53:53 +0000},  Doi = {10.1098/rstb.2012.0198},  Journal = {Philos Trans R Soc Lond B Biol Sci},  Journal-Full = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},  Number = {1614},  Pages = {20120198},  Pmid = {23382421},  Pst = {epublish},  Title = {Uncovering epidemiological dynamics in heterogeneous host populations using phylogenetic methods},  Volume = {368},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rstb.2012.0198}}  @article{Zlateva:2005qy,  Abstract = {Human respiratory syncytial virus (HRSV) is the most important cause of acute respiratory disease in infants. Two major subgroups (A and B) have been identified based on antigenic differences in the attachment G protein. Antigenic variation between and within the subgroups may contribute to reinfections with these viruses by evading the host immune responses. To investigate the circulation patterns and mechanisms by which HRSV-B viruses evolve, we analyzed the G protein genetic variability of subgroup B sequences isolated over a 45-year period, including 196 Belgian strains obtained over 22 epidemic seasons (1982 to 2004). Our study revealed that the HRSV-B evolutionary rate (1.95 x 10(-3) nucleotide substitutions/site/year) is similar to that previously estimated for HRSV-A (1.83 x 10(-3) nucleotide substitutions/site/year). However, natural HRSV-B isolates appear to accommodate more drastic changes in their attachment G proteins. The most recent common ancestor of the currently circulating subgroup B strains was estimated to date back to around the year 1949. The divergence between the two major subgroups was calculated to have occurred approximately 350 years ago. Furthermore, we have identified 12 positively selected sites in the G protein ectodomain, suggesting that immune-driven selective pressure operates in certain codon positions. HRSV-A and -B strains have similar phylodynamic patterns: both subgroups are characterized by global spatiotemporal strain dynamics, where the high infectiousness of HRSV permits the rapid geographic spread of novel strain variants.},  Author = {Zlateva, Kalina T and Lemey, Philippe and Mo{\"e}s, Elien and Vandamme, Anne-Mieke and Van Ranst, Marc},  Date-Added = {2012-08-12 16:33:26 +1200},  Date-Modified = {2012-08-12 16:33:26 +1200},  Doi = {10.1128/JVI.79.14.9157-9167.2005},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Amino Acid Sequence; Evolution, Molecular; Genetic Variation; Glycosylation; Molecular Sequence Data; Phylogeny; Respiratory Syncytial Virus, Human; Viral Envelope Proteins},  Month = {Jul},  Number = {14},  Pages = {9157-67},  Pmc = {PMC1168771},  Pmid = {15994810},  Pst = {ppublish},  Title = {Genetic variability and molecular evolution of the human respiratory syncytial virus subgroup B attachment G protein},  Volume = {79},  Year = {2005},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.79.14.9157-9167.2005}}  @article{Zlateva:2004uq,  Abstract = {Human respiratory syncytial virus (HRSV) is the most common etiological agent of acute lower respiratory tract disease in infants and can cause repeated infections throughout life. In this study, we have analyzed nucleotide sequences encompassing 629 bp at the carboxy terminus of the G glycoprotein gene for HRSV subgroup A strains isolated over 47 years, including 112 Belgian strains isolated over 19 consecutive years (1984 to 2002). By using a maximum likelihood method, we have tested the presence of diversifying selection and identified 13 positively selected sites with a posterior probability above 0.5. The sites under positive selection correspond to sites of O glycosylation or to amino acids that were previously described as monoclonal antibody-induced in vitro escape mutants. Our findings suggest that the evolution of subgroup A HRSV G glycoprotein is driven by immune pressure operating in certain codon positions located mainly in the second hypervariable region of the ectodomain. Phylogenetic analysis revealed the prolonged cocirculation of two subgroup A lineages among the Belgian population and the possible extinction of three other lineages. The evolutionary rate of HRSV subgroup A isolates was estimated to be 1.83 x 10(-3) nucleotide substitutions/site/year, projecting the most recent common ancestor back to the early 1940s.},  Author = {Zlateva, Kalina T and Lemey, Philippe and Vandamme, Anne-Mieke and Van Ranst, Marc},  Date-Added = {2012-08-12 16:33:26 +1200},  Date-Modified = {2012-08-12 16:33:26 +1200},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Belgium; Child, Preschool; Evolution, Molecular; Humans; Infant; Infant, Newborn; Molecular Sequence Data; Phylogeny; Respiratory Syncytial Virus Infections; Respiratory Syncytial Virus, Human; Selection, Genetic; Sequence Analysis, DNA; Viral Proteins},  Month = {May},  Number = {9},  Pages = {4675-83},  Pmc = {PMC387670},  Pmid = {15078950},  Pst = {ppublish},  Title = {Molecular evolution and circulation patterns of human respiratory syncytial virus subgroup a: positively selected sites in the attachment g glycoprotein},  Volume = {78},  Year = {2004}}  @article{Nee1994,  Author = {Nee, S. C. and May, R. M. and Harvey, P. H.},  Date-Modified = {2014-07-06 00:57:12 +0000},  Journal = {Philos. Trans. Roy. Soc. London Ser. B},  Pages = {305--311},  Title = {The reconstructed evolutionary process},  Volume = {344},  Year = {1994}}  @article{Morlon2011,  Author = {Morlon, H. and Parsons, T.L. and Plotkin, J.B.},  Journal = {Proc. Nat. Acad. Sci.},  Number = {39},  Pages = {16327--16332},  Publisher = {National Acad Sciences},  Title = {Reconciling molecular phylogenies with the fossil record},  Volume = {108},  Year = {2011}}  @article{Rabosky2007,  Author = {Rabosky, D.L.},  Journal = {Evolution},  Number = {6},  Pages = {1152--1164},  Publisher = {John Wiley \& Sons},  Title = {{Likelihood methods for detecting temporal shifts in diversification rates}},  Volume = {60},  Year = {2007}}  @article{Stadler2012ProcRoyB,  Author = {Etienne, R.S. and Haegeman, B. and Stadler, T. and Aze, T. and Pearson, P.N. and Purvis, A. and Phillimore, A.B.},  Journal = {Proc. Roy. Soc. B},  Publisher = {The Royal Society},  Title = {Diversity-dependence brings molecular phylogenies closer to agreement with the fossil record},  Volume = {doi: 10.1098/rspb.2011.1439},  Year = {2012}}  @article{Stadler2012sky,  Author = {Stadler, Tanja and K{\"u}hnert, Denise and Bonhoeffer, Sebastian and Drummond, Alexei J.},  Date-Modified = {2014-07-06 00:52:42 +0000},  Journal = {Proc. Nat. Acad. Sci.},  Number = {1},  Title = {Birth-death skyline plot reveals temporal changes of epidemic spread in HIV and HCV},  Volume = {110},  Year = {2013}}  @article{Fitzjohn2009,  Author = {FitzJohn, R. G. and Maddison, W. P. and Otto, S. P.},  Date-Modified = {2014-07-06 05:56:17 +0000},  Journal = {Syst. Biol.},  Number = {6},  Pages = {595},  Publisher = {Oxford University Press},  Title = {Estimating trait-dependent speciation and extinction rates from incompletely resolved phylogenies},  Volume = {58},  Year = {2009}}  @article{Fitzjohn2010,  Author = {FitzJohn, R. G.},  Date-Modified = {2014-12-04 01:08:54 +0000},  Journal = {Systematic biology},  Number = {6},  Pages = {619--633},  Publisher = {Oxford University Press},  Title = {Quantitative traits and diversification},  Volume = {59},  Year = {2010}}  @article{Maddison2007,  Author = {Maddison, W. P.},  Date-Modified = {2014-07-06 05:56:22 +0000},  Journal = {Systematic Biology},  Number = {5},  Pages = {701--710},  Publisher = {Taylor \& Francis},  Title = {{Estimating a Binary Character's Effect on Speciation and Extinction}},  Volume = {56},  Year = {2007}}  @article{Kendall1948b,  Author = {Kendall, David G.},  Journal = {Ann. Math. Statist.},  Number = {1},  Pages = {1--15},  Title = {On the generalized ``birth-and-death'' process},  Volume = {19},  Year = {1948}}  @article{Stadler2012MBE,  Author = {Stadler, Tanja and Kouyos, Roger D. and von Wyl, Viktor and Yerly, Sabine and B\"{o}ni, J\"{u}rg and B\"{u}rgisser, Philippe and Klimkait, Thomas and Joos, Beda and Rieder, Philip and Xie, Dong and G\"{u}nthard, Huldrych F. and Drummond, Alexei J. and Bonhoeffer, Sebastian and the Swiss HIV Cohort Study},  Date-Modified = {2014-07-06 00:51:56 +0000},  Journal = {Molecular Biology and Evolution},  Pages = {347-357},  Publisher = {SMBE},  Title = {Estimating the basic reproductive number from viral sequence data},  Volume = {29},  Year = {2012}}  @article{Stadler2011Science-Mammals,  Author = {Meredith, R.W. and Jane{\v{c}}ka, J.E. and Gatesy, J. and Ryder, O.A. and Fisher, C.A. and Teeling, E.C. and Goodbla, A. and Eizirik, E. and Sim{\~a}o, T.L.L. and Stadler, T. and others},  Journal = {Science},  Number = {6055},  Pages = {521--524},  Publisher = {American Association for the Advancement of Science},  Title = {Impacts of the Cretaceous Terrestrial Revolution and KPg Extinction on Mammal Diversification},  Volume = {334},  Year = {2011}}  @article{Stadler2011PNAS,  Author = {Stadler, Tanja},  Journal = {Proc. Nat. Acad. Sci.},  Number = {15},  Pages = {6187-6192},  Title = {Mammalian phylogeny reveals recent diversification rate shifts},  Volume = {108},  Year = {2011}}  @article{Stadler2012POV,  Author = {Stadler, Tanja},  Date-Modified = {2013-08-30 04:01:51 +0000},  Journal = {Systematic biology},  Number = {2},  Pages = {321--329},  Title = {How can we improve accuracy of macroevolutionary rate estimates?},  Volume = {62},  Year = {2013}}  @article{Wu:2011fk,  Abstract = {We provide a framework for Bayesian coalescent inference from microsatellite data that enables inference of population history parameters averaged over microsatellite mutation models. To achieve this we first implemented a rich family of microsatellite mutation models and related components in the software package BEAST. BEAST is a powerful tool that performs Bayesian MCMC analysis on molecular data to make coalescent and evolutionary inferences. Our implementation permits the application of existing nonparametric methods to microsatellite data. The implemented microsatellite models are based on the replication slippage mechanism and focus on three properties of microsatellite mutation: length dependency of mutation rate, mutational bias toward expansion or contraction, and number of repeat units changed in a single mutation event. We develop a new model that facilitates microsatellite model averaging and Bayesian model selection by transdimensional MCMC. With Bayesian model averaging, the posterior distributions of population history parameters are integrated across a set of microsatellite models and thus account for model uncertainty. Simulated data are used to evaluate our method in terms of accuracy and precision of estimation and also identification of the true mutation model. Finally we apply our method to a red colobus monkey data set as an example.},  Author = {Wu, Chieh-Hsi and Drummond, Alexei J},  Date-Added = {2012-05-24 01:32:01 +0000},  Date-Modified = {2012-05-24 01:32:01 +0000},  Doi = {10.1534/genetics.110.125260},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Animals; Colobus; Computer Simulation; Genealogy and Heraldry; Genetic Loci; Humans; Markov Chains; Microsatellite Repeats; Models, Genetic; Monte Carlo Method; Mutation; Population Dynamics},  Month = {May},  Number = {1},  Pages = {151-64},  Pmc = {PMC3120151},  Pmid = {21385725},  Pst = {ppublish},  Title = {Joint inference of microsatellite mutation models, population history and genealogies using transdimensional Markov Chain Monte Carlo},  Volume = {188},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.110.125260}}  @article{LevinsonGutman1987,  Author = {Levinson, G. and Gutman, G. A.},  Date-Added = {2012-05-24 01:25:14 +0000},  Date-Modified = {2012-05-24 01:25:14 +0000},  Journal = {Nucleic Acids Research},  Number = {13},  Pages = {5323--5338},  Title = {{High frequencies of short frameshifts in poly-CA/TG tandem repeats borne by bacteriophage M13 in $Escherichia$ $coli$ K-12}},  Volume = {15},  Year = {1987}}  @article{ohta1973,  Author = {Ohta, T. and Kimura, M.},  Date-Added = {2012-05-24 01:24:30 +0000},  Date-Modified = {2012-05-24 01:24:30 +0000},  Journal = {Genetics},  Number = {2},  Pages = {201--204},  Title = {A model of mutation appropriate to estimate the number of electrophoretically detectable alleles in a finite population},  Volume = {22},  Year = {1973}}  @article{RichardPaques1976,  Author = {Richard, G. F. and P\^{a}ques, F.},  Date-Added = {2012-05-24 01:24:22 +0000},  Date-Modified = {2012-05-24 01:24:22 +0000},  Journal = {EMBO Report},  Number = {2},  Pages = {122--126},  Title = {Mini- and microsatellite expansions: the recombination connection},  Volume = {1},  Year = {2000}}  @article{Smith1976,  Author = {Smith, G. P.},  Date-Added = {2012-05-24 01:24:08 +0000},  Date-Modified = {2012-05-24 01:24:08 +0000},  Journal = {Science},  Number = {4227},  Pages = {528--535},  Title = {Evolution of repeated DNA sequences by unequal crossover},  Volume = {191},  Year = {1976}}  @article{Heled:2012fk,  Abstract = {The use of fossil evidence to calibrate divergence time estimation has a long history. More recently, Bayesian Markov chain Monte Carlo has become the dominant method of divergence time estimation, and fossil evidence has been reinterpreted as the specification of prior distributions on the divergence times of calibration nodes. These so-called "soft calibrations" have become widely used but the statistical properties of calibrated tree priors in a Bayesian setting hashave not been carefully investigated. Here, we clarify that calibration densities, such as those defined in BEAST 1.5, do not represent the marginal prior distribution of the calibration node. We illustrate this with a number of analytical results on small trees. We also describe an alternative construction for a calibrated Yule prior on trees that allows direct specification of the marginal prior distribution of the calibrated divergence time, with or without the restriction of monophyly. This method requires the computation of the Yule prior conditional on the height of the divergence being calibrated. Unfortunately, a practical solution for multiple calibrations remains elusive. Our results suggest that direct estimation of the prior induced by specifying multiple calibration densities should be a prerequisite of any divergence time dating analysis.},  Author = {Heled, Joseph and Drummond, Alexei J},  Date-Added = {2012-05-20 12:15:13 +1200},  Date-Modified = {2012-05-20 12:15:13 +1200},  Doi = {10.1093/sysbio/syr087},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Mesh = {Animals; Bayes Theorem; Calibration; Classification; Computer Simulation; Evolution, Molecular; Fossils; Markov Chains; Marsupialia; Models, Genetic; Monte Carlo Method; Papio; Phylogeny},  Month = {Jan},  Number = {1},  Pages = {138-49},  Pmc = {PMC3243734},  Pmid = {21856631},  Pst = {ppublish},  Title = {Calibrated tree priors for relaxed phylogenetics and divergence time estimation},  Volume = {61},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/syr087}}  @article{Li:2012fk,  Abstract = {We describe a procedure for model averaging of relaxed molecular clock models in Bayesian phylogenetics. Our approach allows us to model the distribution of rates of substitution across branches, averaged over a set of models, rather than conditioned on a single model. We implement this procedure and test it on simulated data to show that our method can accurately recover the true underlying distribution of rates. We applied the method to a set of alignments taken from a data set of 12 mammalian species and uncovered evidence that lognormally distributed rates better describe this data set than do exponentially distributed rates. Additionally, our implementation of model averaging permits accurate calculation of the Bayes factor(s) between two or more relaxed molecular clock models. Finally, we introduce a new computational approach for sampling rates of substitution across branches that improves the convergence of our Markov chain Monte Carlo algorithms in this context. Our methods are implemented under the BEAST 1.6 software package, available at http://beast-mcmc.googlecode.com.},  Author = {Li, Wai Lok Sibon and Drummond, Alexei J},  Date-Added = {2012-05-18 14:51:29 +1200},  Date-Modified = {2012-05-18 14:51:29 +1200},  Doi = {10.1093/molbev/msr232},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Month = {Feb},  Number = {2},  Pages = {751-61},  Pmc = {PMC3258040},  Pmid = {21940644},  Pst = {ppublish},  Title = {Model averaging and bayes factor calculation of relaxed molecular clocks in bayesian phylogenetics},  Volume = {29},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msr232}}  @article{belfiore2008multilocus,  Author = {Belfiore, N.M. and Liu, L. and Moritz, C.},  Date-Added = {2012-04-15 21:37:34 +0000},  Date-Modified = {2012-04-15 21:37:34 +0000},  Journal = {Systematic Biology},  Number = {2},  Pages = {294},  Title = {{Multilocus phylogenetics of a rapid radiation in the genus Thomomys (Rodentia: Geomyidae)}},  Volume = {57},  Year = {2008}}  @article{Kuhnert:2011ly,  Abstract = {Epidemic modeling of infectious diseases has a long history in both theoretical and empirical research. However the recent explosion of genetic data has revealed the rapid rate of evolution that many populations of infectious agents undergo and has underscored the need to consider both evolutionary and ecological processes on the same time scale. Mathematical epidemiology has applied dynamical models to study infectious epidemics, but these models have tended not to exploit - or take into account - evolutionary changes and their effect on the ecological processes and population dynamics of the infectious agent. On the other hand, statistical phylogenetics has increasingly been applied to the study of infectious agents. This approach is based on phylogenetics, molecular clocks, genealogy-based population genetics and phylogeography. Bayesian Markov chain Monte Carlo and related computational tools have been the primary source of advances in these statistical phylogenetic approaches. Recently the first tentative steps have been taken to reconcile these two theoretical approaches. We survey the Bayesian phylogenetic approach to epidemic modeling of infection diseases and describe the contrasts it provides to mathematical epidemiology as well as emphasize the significance of the future unification of these two fields.},  Author = {K{\"u}hnert, Denise and Wu, Chieh-Hsi and Drummond, Alexei J},  Date-Added = {2011-09-29 01:43:57 +0000},  Date-Modified = {2011-09-29 01:43:57 +0000},  Doi = {10.1016/j.meegid.2011.08.005},  Journal = {Infect Genet Evol},  Journal-Full = {Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases},  Month = {Aug},  Pmid = {21906695},  Pst = {aheadofprint},  Title = {Phylogenetic and epidemic modeling of rapidly evolving infectious diseases},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.meegid.2011.08.005}}  @article{Hey:2010zr,  Abstract = {A method for studying the divergence of multiple closely related populations is described and assessed. The approach of Hey and Nielsen (2007, Integration within the Felsenstein equation for improved Markov chain Monte Carlo methods in population genetics. Proc Natl Acad Sci USA. 104:2785-2790) for fitting an isolation-with-migration model was extended to the case of multiple populations with a known phylogeny. Analysis of simulated data sets reveals the kinds of history that are accessible with a multipopulation analysis. Necessarily, processes associated with older time periods in a phylogeny are more difficult to estimate; and histories with high levels of gene flow are particularly difficult with more than two populations. However, for histories with modest levels of gene flow, or for very large data sets, it is possible to study large complex divergence problems that involve multiple closely related populations or species.},  Author = {Hey, Jody},  Date-Added = {2011-09-29 01:37:45 +0000},  Date-Modified = {2011-09-29 01:37:45 +0000},  Doi = {10.1093/molbev/msp296},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Computer Simulation; Emigration and Immigration; Genetics, Population; Models, Genetic; Phylogeny},  Month = {Apr},  Number = {4},  Pages = {905-20},  Pmc = {PMC2877539},  Pmid = {19955477},  Pst = {ppublish},  Title = {Isolation with migration models for more than two populations},  Volume = {27},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msp296}}  @article{Liu:2009ys,  Abstract = {The estimation of species trees (phylogenies) is one of the most important problems in evolutionary biology, and recently, there has been greater appreciation of the need to estimate species trees directly rather than using gene trees as a surrogate. A Bayesian method constructed under the multispecies coalescent model can consistently estimate species trees but involves intensive computation, which can hinder its application to the phylogenetic analysis of large-scale genomic data. Many summary statistics-based approaches, such as shallowest coalescences (SC) and Global LAteSt Split (GLASS), have been developed to infer species phylogenies for multilocus data sets. In this paper, we propose 2 methods, species tree estimation using average ranks of coalescences (STAR) and species tree estimation using average coalescence times (STEAC), based on the summary statistics of coalescence times. It can be shown that the 2 methods are statistically consistent under the multispecies coalescent model. STAR uses the ranks of coalescences and is thus resistant to variable substitution rates along the branches in gene trees. A simulation study suggests that STAR consistently outperforms STEAC, SC, and GLASS when the substitution rates among lineages are highly variable. Two real genomic data sets were analyzed by the 2 methods and produced species trees that are consistent with previous results.},  Author = {Liu, Liang and Yu, Lili and Pearl, Dennis K and Edwards, Scott V},  Date-Added = {2011-09-29 01:23:05 +0000},  Date-Modified = {2011-09-29 01:23:05 +0000},  Doi = {10.1093/sysbio/syp031},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Mesh = {Algorithms; Classification; Computational Biology; Computer Simulation; Evolution, Molecular; Models, Genetic; Phylogeny; Time Factors},  Month = {Oct},  Number = {5},  Pages = {468-77},  Pmid = {20525601},  Pst = {ppublish},  Title = {Estimating species phylogenies using coalescence times among sequences},  Volume = {58},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/syp031}}  @article{Liu:2009vn,  Abstract = {We review recent models to estimate phylogenetic trees under the multispecies coalescent. Although the distinction between gene trees and species trees has come to the fore of phylogenetics, only recently have methods been developed that explicitly estimate species trees. Of the several factors that can cause gene tree heterogeneity and discordance with the species tree, deep coalescence due to random genetic drift in branches of the species tree has been modeled most thoroughly. Bayesian approaches to estimating species trees utilizes two likelihood functions, one of which has been widely used in traditional phylogenetics and involves the model of nucleotide substitution, and the second of which is less familiar to phylogeneticists and involves the probability distribution of gene trees given a species tree. Other recent parametric and nonparametric methods for estimating species trees involve parsimony criteria, summary statistics, supertree and consensus methods. Species tree approaches are an appropriate goal for systematics, appear to work well in some cases where concatenation can be misleading, and suggest that sampling many independent loci will be paramount. Such methods can also be challenging to implement because of the complexity of the models and computational time. In addition, further elaboration of the simplest of coalescent models will be required to incorporate commonly known issues such as deviation from the molecular clock, gene flow and other genetic forces.},  Author = {Liu, Liang and Yu, Lili and Kubatko, Laura and Pearl, Dennis K and Edwards, Scott V},  Date-Added = {2011-09-29 01:23:00 +0000},  Date-Modified = {2011-09-29 01:23:00 +0000},  Doi = {10.1016/j.ympev.2009.05.033},  Journal = {Mol Phylogenet Evol},  Journal-Full = {Molecular phylogenetics and evolution},  Mesh = {Bayes Theorem; Evolution, Molecular; Genetic Speciation; Likelihood Functions; Models, Genetic; Phylogeny; Sequence Analysis, DNA; Statistics, Nonparametric},  Month = {Oct},  Number = {1},  Pages = {320-8},  Pmid = {19501178},  Pst = {ppublish},  Title = {Coalescent methods for estimating phylogenetic trees},  Volume = {53},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ympev.2009.05.033}}  @article{Liu:2008kx,  Abstract = {Several techniques, such as concatenation and consensus methods, are available for combining data from multiple loci to produce a single statement of phylogenetic relationships. However, when multiple alleles are sampled from individual species, it becomes more challenging to estimate relationships at the level of species, either because concatenation becomes inappropriate due to conflicts among individual gene trees, or because the species from which multiple alleles have been sampled may not form monophyletic groups in the estimated tree. We propose a Bayesian hierarchical model to reconstruct species trees from multiple-allele, multilocus sequence data, building on a recently proposed method for estimating species trees from single allele multilocus data. A two-step Markov Chain Monte Carlo (MCMC) algorithm is adopted to estimate the posterior distribution of the species tree. The model is applied to estimate the posterior distribution of species trees for two multiple-allele datasets--yeast (Saccharomyces) and birds (Manacus-manakins). The estimates of the species trees using our method are consistent with those inferred from other methods and genetic markers, but in contrast to other species tree methods, it provides credible regions for the species tree. The Bayesian approach described here provides a powerful framework for statistical testing and integration of population genetics and phylogenetics.},  Author = {Liu, Liang and Pearl, Dennis K and Brumfield, Robb T and Edwards, Scott V},  Date-Added = {2011-09-29 01:22:52 +0000},  Date-Modified = {2011-09-29 01:22:52 +0000},  Doi = {10.1111/j.1558-5646.2008.00414.x},  Journal = {Evolution},  Journal-Full = {Evolution; international journal of organic evolution},  Mesh = {Algorithms; Alleles; Animals; Bayes Theorem; Biological Evolution; Birds; Computer Simulation; Markov Chains; Models, Genetic; Models, Statistical; Models, Theoretical; Monte Carlo Method; Phylogeny; Saccharomyces cerevisiae; Sequence Analysis, DNA; Species Specificity},  Month = {Aug},  Number = {8},  Pages = {2080-91},  Pmid = {18462214},  Pst = {ppublish},  Title = {Estimating species trees using multiple-allele DNA sequence data},  Volume = {62},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1558-5646.2008.00414.x}}  @article{Edwards:2007uq,  Abstract = {The vast majority of phylogenetic models focus on resolution of gene trees, despite the fact that phylogenies of species in which gene trees are embedded are of primary interest. We analyze a Bayesian model for estimating species trees that accounts for the stochastic variation expected for gene trees from multiple unlinked loci sampled from a single species history after a coalescent process. Application of the model to a 106-gene data set from yeast shows that the set of gene trees recovered by statistically acknowledging the shared but unknown species tree from which gene trees are sampled is much reduced compared with treating the history of each locus independently of an overarching species tree. The analysis also yields a concentrated posterior distribution of the yeast species tree whose mode is congruent with the concatenated gene tree but can do so with less than half the loci required by the concatenation method. Using simulations, we show that, with large numbers of loci, highly resolved species trees can be estimated under conditions in which concatenation of sequence data will positively mislead phylogeny, and when the proportion of gene trees matching the species tree is <10%. However, when gene tree/species tree congruence is high, species trees can be resolved with just two or three loci. These results make accessible an alternative paradigm for combining data in phylogenomics that focuses attention on the singularity of species histories and away from the idiosyncrasies and multiplicities of individual gene histories.},  Author = {Edwards, Scott V and Liu, Liang and Pearl, Dennis K},  Date-Added = {2011-09-29 01:22:48 +0000},  Date-Modified = {2011-09-29 01:22:48 +0000},  Doi = {10.1073/pnas.0607004104},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Alleles; Base Composition; Base Sequence; Bayes Theorem; DNA, Concatenated; DNA, Fungal; Genomics; Likelihood Functions; Markov Chains; Models, Genetic; Models, Statistical; Molecular Sequence Data; Monte Carlo Method; Phylogeny; Saccharomyces cerevisiae; Sequence Analysis, DNA; Species Specificity; Stochastic Processes},  Month = {Apr},  Number = {14},  Pages = {5936-41},  Pmc = {PMC1851595},  Pmid = {17392434},  Pst = {ppublish},  Title = {High-resolution species trees without concatenation},  Volume = {104},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0607004104}}  @article{Heled:2010fk,  Abstract = {Until recently, it has been common practice for a phylogenetic analysis to use a single gene sequence from a single individual organism as a proxy for an entire species. With technological advances, it is now becoming more common to collect data sets containing multiple gene loci and multiple individuals per species. These data sets often reveal the need to directly model intraspecies polymorphism and incomplete lineage sorting in phylogenetic estimation procedures. For a single species, coalescent theory is widely used in contemporary population genetics to model intraspecific gene trees. Here, we present a Bayesian Markov chain Monte Carlo method for the multispecies coalescent. Our method coestimates multiple gene trees embedded in a shared species tree along with the effective population size of both extant and ancestral species. The inference is made possible by multilocus data from multiple individuals per species. Using a multiindividual data set and a series of simulations of rapid species radiations, we demonstrate the efficacy of our new method. These simulations give some insight into the behavior of the method as a function of sampled individuals, sampled loci, and sequence length. Finally, we compare our new method to both an existing method (BEST 2.2) with similar goals and the supermatrix (concatenation) method. We demonstrate that both BEST and our method have much better estimation accuracy for species tree topology than concatenation, and our method outperforms BEST in divergence time and population size estimation.},  Author = {Heled, Joseph and Drummond, Alexei J},  Date-Added = {2011-09-29 01:20:13 +0000},  Date-Modified = {2011-09-29 01:20:13 +0000},  Doi = {10.1093/molbev/msp274},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Algorithms; Bayes Theorem; Computer Simulation; Evolution, Molecular; Genes; Models, Genetic; Monte Carlo Method; Phylogeny; Species Specificity},  Month = {Mar},  Number = {3},  Pages = {570-80},  Pmc = {PMC2822290},  Pmid = {19906793},  Pst = {ppublish},  Title = {Bayesian inference of species trees from multilocus data},  Volume = {27},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msp274}}  @article{Felsenstein:2001fk,  Author = {Felsenstein, J},  Date-Added = {2011-09-27 19:44:58 +1300},  Date-Modified = {2011-09-27 19:44:58 +1300},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Mesh = {Biometry; Classification; History, 20th Century; Humans; Periodicals as Topic; Phylogeny; Societies, Scientific},  Month = {Aug},  Number = {4},  Pages = {465-7},  Pmid = {12116645},  Pst = {ppublish},  Title = {The troubled growth of statistical phylogenetics},  Volume = {50},  Year = {2001}}  @article{Abrahams:2009gb,  Abstract = {Identifying the specific genetic characteristics of successfully transmitted variants may prove central to the development of effective vaccine and microbicide interventions. Although human immunodeficiency virus transmission is associated with a population bottleneck, the extent to which different factors influence the diversity of transmitted viruses is unclear. We estimate here the number of transmitted variants in 69 heterosexual men and women with primary subtype C infections. From 1,505 env sequences obtained using a single genome amplification approach we show that 78\% of infections involved single variant transmission and 22\% involved multiple variant transmissions (median of 3). We found evidence for mutations selected for cytotoxic-T-lymphocyte or antibody escape and a high prevalence of recombination in individuals infected with multiple variants representing another potential escape pathway in these individuals. In a combined analysis of 171 subtype B and C transmission events, we found that infection with more than one variant does not follow a Poisson distribution, indicating that transmission of individual virions cannot be seen as independent events, each occurring with low probability. While most transmissions resulted from a single infectious unit, multiple variant transmissions represent a significant fraction of transmission events, suggesting that there may be important mechanistic differences between these groups that are not yet understood.},  Author = {Abrahams, M-R and Anderson, J A and Giorgi, E E and Seoighe, C and Mlisana, K and Ping, L-H and Athreya, G S and Treurnicht, F K and Keele, B F and Wood, N and Salazar-Gonzalez, J F and Bhattacharya, T and Chu, H and Hoffman, I and Galvin, S and Mapanje, C and Kazembe, P and Thebus, R and Fiscus, S and Hide, W and Cohen, M S and Karim, S Abdool and Haynes, B F and Shaw, G M and Hahn, B H and Korber, B T and Swanstrom, R and Williamson, C and {CAPRISA Acute Infection Study Team} and {Center for HIV-AIDS Vaccine Immunology Consortium}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.02132-08},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Adult; Cluster Analysis; Female; Genetic Variation; HIV Infections; HIV-1; Humans; Male; Molecular Sequence Data; Phylogeny; RNA, Viral; Sequence Analysis, DNA; Sequence Homology; Young Adult},  Month = {Apr},  Number = {8},  Pages = {3556-67},  Pmc = {PMC2663249},  Pmid = {19193811},  Pst = {ppublish},  Title = {Quantitating the multiplicity of infection with human immunodeficiency virus type 1 subtype C reveals a non-poisson distribution of transmitted variants},  Volume = {83},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.02132-08}}  @article{Aguas:2008kx,  Abstract = {Background: A characteristic of Plasmodium falciparum infections is the gradual acquisition of clinical immunity resulting from repeated exposures to the parasite. While the molecular basis of protection against clinical malaria remains unresolved, its effects on epidemiological patterns are well recognized. Accumulating epidemiological data constitute a valuable resource that must be intensively explored and interpreted as to effectively inform control planning.  Methodology/Principal Finding: Here we apply a mathematical model to clinical data from eight endemic regions in sub-Saharan Africa. The model provides a quantitative framework within which differences in age distribution of clinical disease are assessed in terms of the parameters underlying transmission. The shorter infectious periods estimated for clinical infections induce a regime of bistability of endemic and malaria-free states in regions of mesoendemic transmission. The two epidemiological states are separated by a threshold that provides a convenient measure for intervention design. Scenarios of eradication and resurgence are simulated.  Conclusions/Significance: In regions that support mesoendemic transmission, intervention success depends critically on reducing prevalence below a threshold which separates endemic and malaria-free regimes.},  Address = {185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA},  Author = {Aguas, Ricardo and White, Lisa J. and Snow, Robert W. and Gomes, M. Gabriela M.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {DOI 10.1371/journal.pone.0001767},  Isi = {000260723000021},  Isi-Recid = {176781565},  Isi-Ref-Recids = {185773132 148518873 123544640 119553116 25912464 155170202 96492842 110197893 134137814 76552927 129408645 109027704 78812488 143404014 157832698 135991031 114697347 120773122 123335734 43395276 144207142 143373098 109429232 151685071 147390612 151685070 136171402 155593349 142327816 106334009 100690914 185773133 128116040 143205154 131791913 143565999},  Journal = {Plos One},  Month = mar,  Number = {3},  Publisher = {PUBLIC LIBRARY SCIENCE},  Times-Cited = {14},  Title = {Prospects for Malaria Eradication in Sub-Saharan Africa},  Volume = {3},  Year = {2008},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=000260723000021}}  @article{Alizon:2008fk,  Abstract = {There is ample theoretical and experimental evidence that virulence evolution depends on the immune response of the host. In this article, we review a number of recent studies that attempt to explicitly incorporate the dynamics of the immune system (instead of merely representing it by a single black box parameter) in models for the evolution of parasite virulence. A striking observation is that the type of infection (acute or chronic) is invariably considered to be a constraint that model assumptions have to satisfy rather than as a potential outcome of the interaction of the parasite with its host's immune system. We argue that avoiding making assumptions about the type of infection will lead to a better understanding of infectious diseases, even though a number of fundamental and technical problems remain. Dynamical modeling of the immune system opens a wide range of perspectives: for understanding how the immune system eradicates a parasite (which it does for most pathogens but not for all, HIV being a notorious example of a virus that is not completely eliminated), for studying multiple infections through concomitant immunity, for understanding the emergence and evolution of the immune system in animals, and for evolutionary epidemiology in general (e.g., predicting evolutionary consequences of new therapies and public health policies). We conclude by discussing new approaches based on embedded (or nested) models and identify future perspectives for the modeling of infectious diseases.},  Author = {Alizon, Samuel and van Baalen, Minus},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1086/592404},  Journal = {Am Nat},  Journal-Full = {The American naturalist},  Mesh = {Animals; Evolution; Host-Parasite Interactions; Infection; Models, Immunological; Parasites; Virulence},  Month = {Dec},  Number = {6},  Pages = {E244-56},  Pmid = {18999939},  Pst = {ppublish},  Title = {Acute or chronic? Within-host models with immune dynamics, infection outcome, and parasite evolution},  Volume = {172},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1086/592404}}  @article{Alizon:2009kc,  Abstract = {The evolution of infectious diseases is known to affect epidemiological dynamics, but, for some viruses and bacteria, this evolution also takes place inside a host during the course of an infection. I develop an original approach to study intrahost evolutionary dynamics of quantitative disease traits. This approach can be expressed mathematically using the 'Price equation' framework recently developed in evolutionary epidemiology. This framework combines population genetics and within-host population dynamics models to identify trade-offs that affect disease intrahost evolution and to predict short-term evolutionary dynamics of life-history traits. I show that this can be applied to study the evolution of viruses competing for host cells or to study the coevolution between parasites and the immune system of the host. This framework can also easily incorporate experimental data. Studying intrahost evolutionary dynamics provides insight at the within-host level, because it allows us to better understand the course of chronic infections, and at the epidemiological level, because it helps to study multi-scale evolutionary processes. This framework can be used to address important biological issues, from immune escape to disease evolutionary response to treatments.},  Address = {COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA},  Author = {Alizon, S.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {DOI 10.1111/j.1420-9101.2009.01726.x},  Isi = {000265252100019},  Isi-Recid = {179401790},  Isi-Ref-Recids = {146582375 174659713 172566528 47408429 151651302 158162295 133356842 88166683 126418611 116672276 77334338 175891034 157951054 134240761 142091813 166765748 158715517 67588598 95368181 158956028 120290083 179401791 122646587 154316430 99596887 135481732 135864188 96162322 116861210 79833879 137433043 132721207 130209984 136121355 152518920 88223055 87553721 7714584 133954344 136610747 25480153 153312230 173231867 118599565 74249370 121437428 125974332 18381056 151244322 156328432 156923498 160625758 146234435},  Journal = {Journal of Evolutionary Biology},  Keywords = {co-evolution; immune system; infectious diseases; trade-offs; within-host dynamics},  Month = may,  Number = {5},  Pages = {1123-1132},  Publisher = {WILEY-BLACKWELL PUBLISHING, INC},  Times-Cited = {1},  Title = {The Price equation framework to study disease within-host evolution},  Volume = {22},  Year = {2009},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=000265252100019}}  @article{alizon:2010ph,  Author = {Alizon, Samuel and von Wyl, Viktor and Stadler, Tanja and Kouyos, Roger D. and Yerly, Sabine and Hirschel, Bernard and B{\"o}ni, J{\"u}rg and Shah, Cyril and Klimkait, Thomas and Furrer, Hansjakob and Rauch, Andri and Vernazza, Pietro L. and Bernasconi, Enos and Battegay, Manuel and B{\"u}rgisser, Philippe and Telenti, Amalio and G{\"u}nthard, Huldrych F. and Bonhoeffer, Sebastian and the Swiss {HIV} Cohort Study},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.ppat.1001123},  Editor = {Wilke, Claus O.},  Issn = {1553-7374},  Journal = {{PLoS} Pathogens},  Number = {9},  Pages = {e1001123},  Title = {Phylogenetic Approach Reveals That Virus Genotype Largely Determines {HIV} {Set-Point} Viral Load},  Url = {http://www.plospathogens.org.ezproxy.auckland.ac.nz/article/citationList.action;jsessionid=07870CC7530C74CED46107DA2410713F.ambra02?articleURI=info%3Adoi%2F10.1371%2Fjournal.ppat.1001123},  Volume = {6},  Year = {2010},  Bdsk-Url-1 = {http://www.plospathogens.org.ezproxy.auckland.ac.nz/article/citationList.action;jsessionid=07870CC7530C74CED46107DA2410713F.ambra02?articleURI=info:doi/10.1371/journal.ppat.1001123},  Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.ppat.1001123}}  @article{ANDERSON:1982fk,  Address = {40 WEST 20TH STREET, NEW YORK, NY 10011-4211},  Author = {Anderson, RM and May, RM},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Isi = {A1982PP03200017},  Isi-Recid = {47408429},  Isi-Ref-Recids = {37789052 42182178 42793815 45066781 47408430 47408431 38968946 41764135 44727174 27498767 35835963 25086342 36565308 38671788 38362406 10844422 42443700 27153730 44261138 3487253 47408432 41364218 47408433 47408434 38826152 47408435 5159064 1745051 31342862 47408436 42443699 44787025 44787028 47408437 29530084 40993837 37836932 27913126 5346338 31074097 12496693 14996952 47408438 39323871 37884525 23851863 28507142 28273818 36464225 34685156 21623724},  Journal = {Parasitology},  Number = {OCT},  Pages = {411--426},  Publisher = {CAMBRIDGE UNIV PRESS},  Times-Cited = {542},  Title = {COEVOLUTION OF HOSTS AND PARASITES},  Volume = {85},  Year = {1982},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=A1982PP03200017}}  @book{Anderson:1991fk,  Address = {Oxford},  Annote = {LDR 01555cam 2200373 a 4500  001 4833577  005 20060726210443.0  008 901010s1991 enka b 001 0 eng c  906 $a7$bcbc$corignew$d1$eocip$f19$gy-gencatlg  955 $aCIP ver. bt06 to SL 01-21-92; jc03 08-11-92  035 $9(DLC) 90014312  010 $a 90014312   020 $a0198545991 (hardback) :$c£60.00 (est.) ($90.00)  040 $aDNLM/DLC$cDLC$dDLC  050 00 $aRA643$b.A56 1991  060 $aWA 110 A549i  082 00 $a614.4$220  100 1 $aAnderson, Roy M.  245 10 $aInfectious diseases of humans :$bdynamics and control /$cRoy M. Anderson and Robert M. May.  260 $aOxford ;$aNew York :$bOxford University Press,$c1991.  300 $aviii, 757 p. :$bill. ;$c24 cm.  440 0 $aOxford science publications  504 $aIncludes bibliographical references (p. [697]-735) and indexes.  650 0 $aCommunicable diseases$xEpidemiology$xMathematical models.  650 0 $aMicrobial ecology$xMathematical models.  650 2 $aCommunicable Disease Control.  650 2 $aCommunicable Diseases$xparasitology.  650 2 $aEpidemiologic Methods.  650 2 $aHost-Parasite Relations.  650 2 $aModels, Theoretical.  700 1 $aMay, Robert M.$q(Robert McCredie),$d1936-  856 42 $3Publisher description$uhttp://www.loc.gov/catdir/enhancements/fy0636/90014312-d.html  856 41 $3Table of contents only$uhttp://www.loc.gov/catdir/enhancements/fy0636/90014312-t.html  991 $bc-GenColl$hRA643$i.A56 1991$p00017319590$tCopy 1$wBOOKS  },  Author = {Anderson, Roy M and May, Robert M},  Call-Number = {RA643},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Dewey-Call-Number = {614.4},  Genre = {Communicable diseases},  Isbn = {0198545991 (hardback)},  Library-Id = {90014312},  Publisher = {Oxford University Press},  Title = {Infectious diseases of humans: dynamics and control},  Url = {http://www.loc.gov/catdir/enhancements/fy0636/90014312-d.html},  Year = {1991},  Bdsk-Url-1 = {http://www.loc.gov/catdir/enhancements/fy0636/90014312-d.html}}  @article{antonovics:2006mo,  Abstract = {Taubenberger et al. claim that the 1918 influenza virus was derived from an avian source and adapted to humans shortly before the pandemic. However, we do not believe that this conclusion, which has been widely disseminated in the popular press and in scientific journals, is supported by their phylogenetic evidence.},  Author = {Antonovics, Janis and Hood, Michael E and Baker, Christi Howell},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nature04824},  Issn = {1476-4687},  Journal = {Nature},  Keywords = {Animals, Birds, Evolution, Molecular, History, 20th Century, Humans, Influenza A Virus, {H1N1} Subtype, Influenza in Birds, Influenza, Human, Models, Biological, Phylogeny, Reproducibility of Results, Swine, Time Factors, Zoonoses},  Month = apr,  Note = {{PMID:} 16641950},  Number = {7088},  Pages = {E9; discussion E9--10},  Title = {Molecular virology: was the 1918 flu avian in origin?},  Url = {http://www.ncbi.nlm.nih.gov/pubmed/16641950},  Volume = {440},  Year = {2006},  Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed/16641950},  Bdsk-Url-2 = {http://dx.doi.org/10.1038/nature04824}}  @article{aris-brosou:2002ef,  Abstract = {The molecular clock, i.e., constancy of the rate of evolution over time, is commonly assumed in estimating divergence dates. However, this assumption is often violated and has drastic effects on date estimation. Recently, a number of attempts have been made to relax the clock assumption. One approach is to use maximum likelihood, which assigns rates to branches and allows the estimation of both rates and times. An alternative is the Bayes approach, which models the change of the rate over time. A number of models of rate change have been proposed. We have extended and evaluated models of rate evolution, i.e., the lognormal and its recent variant, along with the gamma, the exponential, and the {Ornstein-Uhlenbeck} processes. These models were first applied to a small hominoid data set, where an empirical Bayes approach was used to estimate the hyperparameters that measure the amount of rate variation. Estimation of divergence times was sensitive to these hyperparameters, especially when the assumed model is close to the clock assumption. The rate and date estimates varied little from model to model, although the posterior Bayes factor indicated the {Ornstein-Uhlenbeck} process outperformed the other models. To demonstrate the importance of allowing for rate change across lineages, this general approach was used to analyze a larger data set consisting of the {18S} ribosomal {RNA} gene of 39 metazoan species. We obtained date estimates consistent with paleontological records, the deepest split within the group being about 560 million years ago. Estimates of the rates were in accordance with the Cambrian explosion hypothesis and suggested some more recent lineage-specific bursts of evolution.},  Author = {{Aris-Brosou}, Stephane and Yang, Ziheng},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1080/10635150290102375},  Journal = {Systematic Biology},  Number = {5},  Pages = {703--714},  Title = {Effects of Models of Rate Evolution on Estimation of Divergence Dates with Special Reference to the Metazoan {18S} Ribosomal {RNA} Phylogeny},  Url = {http://sysbio.oxfordjournals.org/cgi/content/abstract/51/5/703},  Volume = {51},  Year = {2002},  Bdsk-Url-1 = {http://sysbio.oxfordjournals.org/cgi/content/abstract/51/5/703},  Bdsk-Url-2 = {http://dx.doi.org/10.1080/10635150290102375}}  @article{aris:2002:ef,  Abstract = {The molecular clock, i.e., constancy of the rate of evolution over time, is commonly assumed in estimating divergence dates. However, this assumption is often violated and has drastic effects on date estimation. Recently, a number of attempts have been made to relax the clock assumption. One approach is to use maximum likelihood, which assigns rates to branches and allows the estimation of both rates and times. An alternative is the Bayes approach, which models the change of the rate over time. A number of models of rate change have been proposed. We have extended and evaluated models of rate evolution, i.e., the lognormal and its recent variant, along with the gamma, the exponential, and the {Ornstein-Uhlenbeck} processes. These models were first applied to a small hominoid data set, where an empirical Bayes approach was used to estimate the hyperparameters that measure the amount of rate variation. Estimation of divergence times was sensitive to these hyperparameters, especially when the assumed model is close to the clock assumption. The rate and date estimates varied little from model to model, although the posterior Bayes factor indicated the {Ornstein-Uhlenbeck} process outperformed the other models. To demonstrate the importance of allowing for rate change across lineages, this general approach was used to analyze a larger data set consisting of the {18S} ribosomal {RNA} gene of 39 metazoan species. We obtained date estimates consistent with paleontological records, the deepest split within the group being about 560 million years ago. Estimates of the rates were in accordance with the Cambrian explosion hypothesis and suggested some more recent lineage-specific bursts of evolution.},  Author = {{Aris-Brosou}, Stephane and Yang, Ziheng},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1080/10635150290102375},  Journal = {Systematic Biology},  Number = {5},  Pages = {703--714},  Title = {Effects of Models of Rate Evolution on Estimation of Divergence Dates with Special Reference to the Metazoan {18S} Ribosomal {RNA} Phylogeny},  Url = {http://sysbio.oxfordjournals.org/cgi/content/abstract/51/5/703},  Volume = {51},  Year = {2002},  Bdsk-Url-1 = {http://sysbio.oxfordjournals.org/cgi/content/abstract/51/5/703},  Bdsk-Url-2 = {http://dx.doi.org/10.1080/10635150290102375}}  @article{Baccam:2006uq,  Abstract = {Currently, little is known about the viral kinetics of influenza A during infection within an individual. We utilize a series of mathematical models of increasing complexity, which incorporate target cell limitation and the innate interferon response, to examine influenza A virus kinetics in the upper respiratory tracts of experimentally infected adults. The models were fit to data from an experimental H1N1 influenza A/Hong Kong/123/77 infection and suggest that it is important to include the eclipse phase of the viral life cycle in viral dynamic models. Doing so, we estimate that after a delay of approximately 6 h, infected cells begin producing influenza virus and continue to do so for approximately 5 h. The average lifetime of infected cells is approximately 11 h, and the half-life of free infectious virus is approximately 3 h. We calculated the basic reproductive number, R(0), which indicated that a single infected cell could produce approximately 22 new productive infections. This suggests that antiviral treatments have a large hurdle to overcome in moderating symptoms and limiting infectiousness and that treatment has to be initiated as early as possible. For about 50\% of patients, the curve of viral titer versus time has two peaks. This bimodal behavior can be explained by incorporating the antiviral effects of interferon into the model. Our model also compared well to an additional data set on viral titer after experimental infection and treatment with the neuraminidase inhibitor zanamivir, which suggests that such models may prove useful in estimating the efficacies of different antiviral therapies for influenza A infection.},  Author = {Baccam, Prasith and Beauchemin, Catherine and Macken, Catherine A and Hayden, Frederick G and Perelson, Alan S},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.01623-05},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Administration, Intranasal; Adult; Antiviral Agents; Guanidines; Humans; Influenza A Virus, H1N1 Subtype; Influenza, Human; Interferons; Kinetics; Models, Theoretical; Nose; Pyrans; Sialic Acids; Zanamivir},  Month = {Aug},  Number = {15},  Pages = {7590-9},  Pmc = {PMC1563736},  Pmid = {16840338},  Pst = {ppublish},  Title = {Kinetics of influenza A virus infection in humans},  Volume = {80},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.01623-05}}  @article{bailes:2003hy,  Author = {Bailes, Elizabeth and Gao, Feng and {Bibollet-Ruche}, Frederic and Courgnaud, Valerie and Peeters, Martine and Marx, Preston A. and Hahn, Beatrice H. and Sharp, Paul M.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1080657},  Journal = {Science},  Month = jun,  Number = {5626},  Pages = {1713},  Title = {Hybrid Origin of {SIV} in Chimpanzees},  Url = {http://www.sciencemag.org},  Volume = {300},  Year = {2003},  Bdsk-Url-1 = {http://www.sciencemag.org},  Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.1080657}}  @article{Barton:2002fk,  Abstract = {We introduce a general recursion for the probability of identity in state of two individuals sampled from a population subject to mutation, migration, and random drift in a two-dimensional continuum. The recursion allows for the interactions induced by density-dependent regulation of the population, which are inevitable in a continuous population. We give explicit series expansions for large neighbourhood size and for low mutation rates respectively and investigate the accuracy of the classical Mal{\'e}cot formula for these general models. When neighbourhood size is small, this formula does not give the identity even over large scales. However, for large neighbourhood size, it is an accurate approximation which summarises the local population structure in terms of three quantities: the effective dispersal rate, sigma(e); the effective population density, rho(e); and a local scale, kappa, at which local interactions become significant. The results are illustrated by simulations.},  Author = {Barton, Nick H and Depaulis, Frantz and Etheridge, Alison M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1006/tpbi.2001.1557},  Journal = {Theor Popul Biol},  Journal-Full = {Theoretical population biology},  Mesh = {Alleles; Animal Migration; Animals; Biological Evolution; Data Interpretation, Statistical; Models, Biological; Mutation; Population Density; Population Dynamics},  Month = {Feb},  Number = {1},  Pages = {31-48},  Pmid = {11895381},  Pst = {ppublish},  Title = {Neutral evolution in spatially continuous populations},  Volume = {61},  Year = {2002},  Bdsk-Url-1 = {http://dx.doi.org/10.1006/tpbi.2001.1557}}  @article{Barton:2010,  Author = {Barton, Nick H and Etheridge, Alison M and Veber, Amandine},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Electronic Journal of Probability},  Pages = {162-216},  Title = {A new model for evolution in a spatial continuum},  Volume = {15},  Year = {2010}}  @article{Barton:2010kx,  Abstract = {Classical models of gene flow fail in three ways: they cannot explain large-scale patterns; they predict much more genetic diversity than is observed; and they assume that loosely linked genetic loci evolve independently. We propose a new model that deals with these problems. Extinction events kill some fraction of individuals in a region. These are replaced by offspring from a small number of parents, drawn from the preexisting population. This model of evolution forwards in time corresponds to a backwards model, in which ancestral lineages jump to a new location if they are hit by an event, and may coalesce with other lineages that are hit by the same event. We derive an expression for the identity in allelic state, and show that, over scales much larger than the largest event, this converges to the classical value derived by Wright and Mal{\'e}cot. However, rare events that cover large areas cause low genetic diversity, large-scale patterns, and correlations in ancestry between unlinked loci.},  Author = {Barton, Nicholas H and Kelleher, Jerome and Etheridge, Alison M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1558-5646.2010.01019.x},  Journal = {Evolution},  Journal-Full = {Evolution; international journal of organic evolution},  Mesh = {Extinction, Biological; Gene Flow; Genetic Variation; Geography; Models, Genetic; Phylogeny; Population Dynamics},  Month = {Sep},  Number = {9},  Pages = {2701-15},  Pmid = {20408876},  Pst = {ppublish},  Title = {A new model for extinction and recolonization in two dimensions: quantifying phylogeography},  Volume = {64},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1558-5646.2010.01019.x}}  @article{Bedford:2010fk,  Abstract = {The global migration patterns of influenza viruses have profound implications for the evolutionary and epidemiological dynamics of the disease. We developed a novel approach to reconstruct the genetic history of human influenza A (H3N2) collected worldwide over 1998 to 2009 and used it to infer the global network of influenza transmission. Consistent with previous models, we find that China and Southeast Asia lie at the center of this global network. However, we also find that strains of influenza circulate outside of Asia for multiple seasons, persisting through dynamic migration between northern and southern regions. The USA acts as the primary hub of temperate transmission and, together with China and Southeast Asia, forms the trunk of influenza's evolutionary tree. These findings suggest that antiviral use outside of China and Southeast Asia may lead to the evolution of long-term local and potentially global antiviral resistance. Our results might also aid the design of surveillance efforts and of vaccines better tailored to different geographic regions.},  Author = {Bedford, Trevor and Cobey, Sarah and Beerli, Peter and Pascual, Mercedes},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.ppat.1000918},  Journal = {PLoS Pathog},  Journal-Full = {PLoS pathogens},  Mesh = {Asia; Emigration and Immigration; Evolution, Molecular; Genetic Variation; Geographic Information Systems; Humans; Influenza A Virus, H3N2 Subtype; Influenza, Human; Pedigree; United States; World Health},  Month = {May},  Number = {5},  Pages = {e1000918},  Pmc = {PMC2877742},  Pmid = {20523898},  Pst = {epublish},  Title = {Global migration dynamics underlie evolution and persistence of human influenza A (H3N2)},  Volume = {6},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.ppat.1000918}}  @article{beerli:2004ef,  Abstract = {Current estimators of gene flow come in two methods; those that estimate parameters assuming that the populations investigated are a small random sample of a large number of populations and those that assume that all populations were sampled. Maximum likelihood or Bayesian approaches that estimate the migration rates and population sizes directly using coalescent theory can easily accommodate datasets that contain a population that has no data, a so-called 'ghost' population. This manipulation allows us to explore the effects of missing populations on the estimation of population sizes and migration rates between two specific populations. The biases of the inferred population parameters depend on the magnitude of the migration rate from the unknown populations. The effects on the population sizes are larger than the effects on the migration rates. The more immigrants from the unknown populations that are arriving in the sample populations the larger the estimated population sizes. Taking into account a ghost population improves or at least does not harm the estimation of population sizes. Estimates of the scaled migration rate M (migration rate per generation divided by the mutation rate per generation) are fairly robust as long as migration rates from the unknown populations are not huge. The inclusion of a ghost population does not improve the estimation of the migration rate M; when the migration rates are estimated as the number of immigrants Nm then a ghost population improves the estimates because of its effect on population size estimation. It seems that for 'real world' analyses one should carefully choose which populations to sample, but there is no need to sample every population in the neighbourhood of a population of interest.},  Author = {Beerli, Peter},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-27 15:34:53 +1300},  Doi = {10.1111/j.1365-294X.2004.02101.x},  Journal = {Molecular Ecology},  Number = {4},  Pages = {827--836},  Title = {Effect of unsampled populations on the estimation of population sizes and migration rates between sampled populations},  Volume = {13},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1111/j.1365-294X.2004.02101.x},  Bdsk-Url-2 = {http://dx.doi.org/10.1111/j.1365-294X.2004.02101.x}}  @article{Bennett:2010fk,  Abstract = {Dengue is an emerging tropical disease infecting tens of millions of people annually. A febrile illness with potentially severe hemorrhagic manifestations, dengue is caused by mosquito-borne viruses (DENV-1 to -4) that are maintained in endemic transmission in large urban centers of the tropics with periodic epidemic cycles at 3- to 5-year intervals. Puerto Rico (PR), a major population center in the Caribbean, has experienced increasingly severe epidemics since multiple dengue serotypes were introduced beginning in the late 1970s. We document the phylodynamics of DENV-4 between 1981 and 1998, a period of dramatic ecological expansion during which evolutionary change also occurs. The timescale of viral evolution is sufficiently short that viral transmission dynamics can be elucidated from genetic diversity data. Specifically, by combining virus sequence data with confirmed case counts in PR over these two decades, we show that the pattern of cyclic epidemics is strongly correlated with coalescent estimates of effective population size that have been estimated from sampled virus sequences using Bayesian Markov Chain Monte Carlo methods. Thus, we show that the observed epidemiologic dynamics are correlated with similar fluctuations in diversity, including severe interepidemic reductions in genetic diversity compatible with population bottlenecks that may greatly impact DENV evolutionary dynamics. Mean effective population sizes based on genetic data appear to increase prior to isolation counts, suggesting a potential bias in the latter and justifying more active surveillance of DENV activity. Our analysis explicitly integrates epidemiologic and sequence data in a joint model that could be used to further explore transmission models of infectious disease.},  Author = {Bennett, S N and Drummond, A J and Kapan, D D and Suchard, M A and Mu{\~n}oz-Jord{\'a}n, J L and Pybus, O G and Holmes, E C and Gubler, D J},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msp285},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Animals; DNA, Viral; Dengue; Dengue Virus; Disease Outbreaks; Evolution; Probability; Puerto Rico},  Month = {Apr},  Number = {4},  Pages = {811-8},  Pmc = {PMC2877535},  Pmid = {19965886},  Pst = {ppublish},  Title = {Epidemic dynamics revealed in dengue evolution},  Volume = {27},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msp285}}  @article{bernard:2007hi,  Abstract = {Phylogenetic analysis 2013 the study of the genetic relatedness between {HIV} strains 2013 has recently been used in criminal prosecutions as evidence of responsibility for {HIV} transmission. In these trials, the expert opinion of virologists has been of critical importance. Phylogenetic analysis of {HIV} gene sequences is complex and its findings do not achieve the levels of certainty obtained with the forensic analysis of human {DNA.} Although two individuals may carry {HIV} strains that are closely related, these will not necessarily be unique to the two parties and could extend to other persons within the same transmission network. For forensic purposes, phylogenetic analysis should be conducted under strictly controlled conditions by laboratories with relevant expertise applying rigorous methods. It is vitally important to include the right controls, which should be epidemiologically and temporally relevant to the parties under investigation. Use of inappropriate controls can exaggerate any relatedness between the virus strains of the complainant and defendant as being strikingly unique. It will be often difficult to obtain the relevant controls. If convenient but less appropriate controls are used, interpretation of the findings should be tempered accordingly. Phylogenetic analysis cannot prove that {HIV} transmission occurred directly between two individuals. However, it can exonerate individuals by demonstrating that the defendant carries a virus strain unrelated to that of the complainant. Expert witnesses should acknowledge the limitations of the inferences that might be made and choose the correct language in both written and verbal testimony.},  Author = {Bernard, E. J. and Azad, Y. and Vandamme, A. M. and Weait, M. and Geretti, A. M.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1468-1293.2007.00486.x},  Journal = {{HIV} Medicine},  Number = {6},  Pages = {382--387},  Shorttitle = {{HIV} forensics},  Title = {{HIV} forensics: pitfalls and acceptable standards in the use of phylogenetic analysis as evidence in criminal investigations of {HIV} transmission},  Url = {http://dx.doi.org/10.1111/j.1468-1293.2007.00486.x},  Volume = {8},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1468-1293.2007.00486.x}}  @article{Biek:2006cr,  Abstract = {Directly transmitted parasites often provide substantial information about the temporal and spatial characteristics of host-to-host contact. Here, we demonstrate that a fast-evolving virus (feline immunodeficiency virus, FIV) can reveal details of the contemporary population structure and recent demographic history of its natural wildlife host (Puma concolor) that were not apparent from host genetic data and would be impossible to obtain by other means. We suggest that rapidly evolving pathogens may provide a complementary tool for studying population dynamics of their hosts in "shallow" time.},  Author = {Biek, Roman and Drummond, Alexei J and Poss, Mary},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1121360},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Alberta; Animals; Bayes Theorem; British Columbia; Ecosystem; Evolution, Molecular; Genes, env; Genes, pol; Geography; Immunodeficiency Virus, Feline; Lentivirus Infections; Microsatellite Repeats; Molecular Sequence Data; Montana; Phylogeny; Population Dynamics; Puma; Time Factors; Wyoming},  Month = {Jan},  Number = {5760},  Pages = {538-41},  Pmid = {16439664},  Pst = {ppublish},  Title = {A virus reveals population structure and recent demographic history of its carnivore host},  Volume = {311},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1121360}}  @article{biek:2007hi,  Author = {Biek, Roman and Henderson, J. Caroline and Waller, Lance A. and Rupprecht, Charles E. and Real, Leslie A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-27 15:39:09 +1300},  Doi = {10.1073/pnas.0700741104},  Journal = {Proceedings of the National Academy of Sciences},  Month = may,  Number = {19},  Pages = {7993 --7998},  Title = {A high-resolution genetic signature of demographic and spatial expansion in epizootic rabies virus},  Volume = {104},  Year = {2007},  Bdsk-Url-1 = {http://www.pnas.org/content/104/19/7993.abstract%20N2%20-%20Emerging%20pathogens%20potentially%20undergo%20rapid%20evolution%20while%20expanding%20in%20population%20size%20and%20geographic%20range%20during%20the%20course%20of%20invasion,%20yet%20it%20is%20generally%20difficult%20to%20demonstrate%20how%20these%20processes%20interact.%20Our%20analysis%20of%20a%2030-yr%20data%20set%20covering%20a%20large-scale%20rabies%20virus%20outbreak%20among%20North%20American%20raccoons%20reveals%20the%20long%20lasting%20effect%20of%20the%20initial%20infection%20wave%20in%20determining%20how%20viral%20populations%20are%20genetically%20structured%20in%20space.%20We%20further%20find%20that%20coalescent-based%20estimates%20derived%20from%20the%20genetic%20data%20yielded%20an%20amazingly%20accurate%20reconstruction%20of%20the%20known%20spatial%20and%20demographic%20dynamics%20of%20the%20virus%20over%20time.%20Our%20study%20demonstrates%20the%20combined%20evolutionary%20and%20population%20dynamic%20processes%20characterizing%20the%20spread%20of%20pathogen%20after%20its%20introduction%20into%20a%20fully%20susceptible%20host%20population.%20Furthermore,%20the%20results%20provide%20important%20insights%20regarding%20the%20spatial%20scale%20of%20rabies%20persistence%20and%20validate%20the%20use%20of%20coalescent%20approaches%20for%20uncovering%20even%20relatively%20complex%20population%20histories.%20Such%20approaches%20will%20be%20of%20increasing%20relevance%20for%20understanding%20the%20epidemiology%20of%20emerging%20zoonotic%20diseases%20in%20a%20landscape%20context.%20ER%20-},  Bdsk-Url-2 = {http://dx.doi.org/10.1073/pnas.0700741104}}  @article{biek:2010la,  Abstract = {Abstract The spread of parasites is inherently a spatial process often embedded in physically complex landscapes. It is therefore not surprising that infectious disease researchers are increasingly taking a landscape genetics perspective to elucidate mechanisms underlying basic ecological processes driving infectious disease dynamics and to understand the linkage between spatially dependent population processes and the geographic distribution of genetic variation within both hosts and parasites. The increasing availability of genetic information on hosts and parasites when coupled to their ecological interactions can lead to insights for predicting patterns of disease emergence, spread and control. Here, we review research progress in this area based on four different motivations for the application of landscape genetics approaches: (i) assessing the spatial organization of genetic variation in parasites as a function of environmental variability, (ii) using host population genetic structure as a means to parameterize ecological dynamics that indirectly influence parasite populations, for example, gene flow and movement pathways across heterogeneous landscapes and the concurrent transport of infectious agents, (iii) elucidating the temporal and spatial scales of disease processes and (iv) reconstructing and understanding infectious disease invasion. Throughout this review, we emphasize that landscape genetic principles are relevant to infection dynamics across a range of scales from within host dynamics to global geographic patterns and that they can also be applied to unconventional `landscapes' such as heterogeneous contact networks underlying the spread of human and livestock diseases. We conclude by discussing some general considerations and problems for inferring epidemiological processes from genetic data and try to identify possible future directions and applications for this rapidly expanding field.},  Author = {{BIEK}, R. and {REAL}, L. A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1365-294X.2010.04679.x},  Issn = {{1365-294X}},  Journal = {Molecular Ecology},  Keywords = {emerging infectious diseases, gene flow, heterogeneity, invasion, molecular epidemiology, parasite},  Pages = {no},  Title = {The landscape genetics of infectious disease emergence and spread},  Url = {http://dx.doi.org/10.1111/j.1365-294X.2010.04679.x},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1365-294X.2010.04679.x}}  @article{Bloom:2007ly,  Abstract = {Naturally evolving proteins gradually accumulate mutations while continuing to fold to stable structures. This process of neutral evolution is an important mode of genetic change and forms the basis for the molecular clock. We present a mathematical theory that predicts the number of accumulated mutations, the index of dispersion, and the distribution of stabilities in an evolving protein population from knowledge of the stability effects (delta deltaG values) for single mutations. Our theory quantitatively describes how neutral evolution leads to marginally stable proteins and provides formulas for calculating how fluctuations in stability can overdisperse the molecular clock. It also shows that the structural influences on the rate of sequence evolution observed in earlier simulations can be calculated using just the single-mutation delta deltaG values. We consider both the case when the product of the population size and mutation rate is small and the case when this product is large, and show that in the latter case the proteins evolve excess mutational robustness that is manifested by extra stability and an increase in the rate of sequence evolution. All our theoretical predictions are confirmed by simulations with lattice proteins. Our work provides a mathematical foundation for understanding how protein biophysics shapes the process of evolution.},  Author = {Bloom, Jesse D and Raval, Alpan and Wilke, Claus O},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1534/genetics.106.061754},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Computer Simulation; Evolution, Molecular; Mathematics; Mutation; Proteins; Thermodynamics},  Month = {Jan},  Number = {1},  Pages = {255-66},  Pmc = {PMC1775007},  Pmid = {17110496},  Pst = {ppublish},  Title = {Thermodynamics of neutral protein evolution},  Volume = {175},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.106.061754}}  @article{bloomquist:2010un,  Author = {Bloomquist, Erik W. and Suchard, Marc A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-29 00:00:53 +0000},  Doi = {10.1093/sysbio/syp076},  Journal = {Systematic Biology},  Month = jan,  Number = {1},  Pages = {27 --41},  Title = {Unifying Vertical and Nonvertical Evolution: A Stochastic {ARG-based} Framework},  Volume = {59},  Year = {2010},  Bdsk-Url-1 = {http://sysbio.oxfordjournals.org/content/59/1/27.abstract},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/sysbio/syp076}}  @article{Bonhoeffer:1997zr,  Abstract = {Analysis of the short-term dynamics of human immunodeficiency virus (HIV) type 1 infection in response to drug therapy has elucidated crucial kinetic properties of viral dynamics in vivo (D. D. Ho et al., Nature 373:123-126, 1995; A. S. Perelson et al., Science 271:1582-1586, 1996; X. Wei et al., Nature 373:117-122, 1995). Here we investigated long-term changes in virus load in patients treated with a combination of lamivudine and zidovudine to identify principal factors responsible for the observed 10- to 100-fold sustained suppression of virus load in vivo. Interestingly, most standard accounts of virus dynamics cannot explain a large sustained reduction without shifting the virus very close to extinction. The effect can be explained by taking into consideration either (i) the immune response against HIV, (ii) the killing of uninfected CD4 cells, or (iii) the differential efficacies of the drugs in different cell populations.},  Author = {Bonhoeffer, S and Coffin, J M and Nowak, M A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Anti-HIV Agents; HIV Infections; HIV-1; Humans; Lamivudine; Reverse Transcriptase Inhibitors; Viral Load; Zidovudine},  Month = {Apr},  Number = {4},  Pages = {3275-8},  Pmc = {PMC191463},  Pmid = {9060694},  Pst = {ppublish},  Title = {Human immunodeficiency virus drug therapy and virus load},  Volume = {71},  Year = {1997}}  @article{BREMERMANN:1989uq,  Address = {175 FIFTH AVE, NEW YORK, NY 10010},  Author = {Bremermann, HJ and Thieme, HR},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Isi = {A1989T943800004},  Isi-Recid = {68681456},  Isi-Ref-Recids = {68681457 37789052 47408429 42793815 51749762 14691929 38063755 68681458 46894062 48218820 48229279 57901056 63400399 59738960 49579198 68681459 68681460 68681461 38671787 68681462 10844422 42443700 27153730 24530210 61711012 68681463 42443699 18782446 48218836 68681464 63164289 50535029 28969665 46373772 3628500 42679190 25320960 65140305},  Journal = {Journal of Mathematical Biology},  Number = {2},  Pages = {179--190},  Publisher = {SPRINGER VERLAG},  Times-Cited = {152},  Title = {A COMPETITIVE-EXCLUSION PRINCIPLE FOR PATHOGEN VIRULENCE},  Volume = {27},  Year = {1989},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=A1989T943800004}}  @article{Britton:2010vn,  Abstract = {This paper is a survey paper on stochastic epidemic models. A simple stochastic epidemic model is defined and exact and asymptotic (relying on a large community) properties are presented. The purpose of modelling is illustrated by studying effects of vaccination and also in terms of inference procedures for important parameters, such as the basic reproduction number and the critical vaccination coverage. Several generalizations towards realism, e.g. multitype and household epidemic models, are also presented, as is a model for endemic diseases. (C) 2010 Elsevier Inc. All rights reserved.},  Address = {360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA},  Author = {Britton, Tom},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {DOI 10.1016/j.mbs.2010.01.006},  Isi = {000277819600004},  Isi-Recid = {188998330},  Isi-Ref-Recids = {117962136 124478108 94901301 103368257 90173742 49445990 85586042 59500641 103207201 27614363 318502 95300111 149230004 12879624 125388123 160650501 161691565 155663390 188998331 116079678 116888313 181478392 150779595 188998332 129381337 125732565 27669480 184528430 5159064 1745051 33771207 109211988 130305098 127210824 73051626 187487907 85586047 56828748 49446022 77943114 40432343 184346803},  Journal = {Mathematical Biosciences},  Keywords = {Basic reproduction number; Critical vaccination coverage; Household epidemic; Multitype epidemic; Stochastic epidemic; Threshold theorem},  Month = may,  Number = {1},  Pages = {24--35},  Publisher = {ELSEVIER SCIENCE INC},  Times-Cited = {1},  Title = {Stochastic epidemic models: A survey},  Volume = {225},  Year = {2010},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=000277819600004}}  @article{Brown:1997uq,  Abstract = {Selection is usually considered to be the dominant force controlling viral variation; the large population sizes suggest that deterministic population genetic models are appropriate. To investigate their validity for HIV, samples of env gene sequences were tested for departure from neutrality because of mutation-selection balance. None of the samples departed significantly when tested as nucleotide sequences. At the amino acid level, significantly elevated diversity was detected in two samples within, but not outside, the V3 loop. The effective population number has been estimated (using a phylogenetic method) to be close to 10(3). Estimates from nucleotide diversity are about 2-fold lower. The low value of the effective population number might arise from high variability in progeny number between infected cells, from the expansion in population number from a small inoculum as the virus is transmitted between hosts, or from variable selection at linked sites. These results suggest that the population genetics of HIV are best described by stochastic models.},  Author = {Brown, A J},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Amino Acid Sequence; Genes, env; Genetic Variation; Genetics, Population; HIV Envelope Protein gp120; HIV Infections; HIV-1; Humans; Models, Genetic; Mutation; Peptide Fragments; RNA, Viral; Spleen; Viremia},  Month = {Mar},  Number = {5},  Pages = {1862-5},  Pmc = {PMC20008},  Pmid = {9050870},  Pst = {ppublish},  Title = {Analysis of HIV-1 env gene sequences reveals evidence for a low effective number in the viral population},  Volume = {94},  Year = {1997}}  @article{brown:2009ph,  Abstract = {Phylogenetic reconstructions of transmission events from individuals with acute human immunodeficiency virus {(HIV)} infection are conducted to illustrate this group's heightened infectivity. Varied definitions of acute infection and assumptions about observed phylogenetic clusters may produce misleading results. We conducted a phylogenetic analysis of {HIV} pol sequences from 165 European patients with estimated infection dates and calculated the difference between dates within clusters. Nine phylogenetic clusters were observed. Comparison of dates within clusters revealed that only 2 could have been generated during acute infection. Previous analyses may have incorrectly assigned transmission events to the acutely {HIV} infected when they were more likely to have occurred during chronic infection.},  Annote = {{PMID:} 19133810},  Author = {Brown, Alison E. and Gifford, Robert J. and Clewley, Jonathan P. and Kucherer, Claudia and Masquelier, Bernard and Porter, Kholoud and Balotta, Claudia and Back, Nicole K. T. and Jorgensen, Louise Bruun and de Mendoza, Carmen and Bhaskaran, Krishnan and Gill, O. Noel and Johnson, Anne M. and Pillay, Deenan},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {The Journal of Infectious Diseases},  Month = feb,  Number = {3},  Pages = {427--431},  Url = {http://dx.doi.org/10.1086/596049},  Volume = {199},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1086/596049}}  @article{buonaguro:2008mo,  Abstract = {{OBJECTIVE:The} continuous identification of {HIV-1} {non-B} subtypes and recombinant forms in Italy indicates the need of constant molecular epidemiology survey of genetic forms circulating and transmitted in the resident {population.METHODS:The} distribution of {HIV-1} subtypes has been evaluated in 25 seropositive individuals residing in Italy, most of whom were infected through a sexual route during the 1995-2005 period. Each sample has been characterized by detailed molecular and phylogenetic {analyses.RESULTS:18} of the 25 samples were positive at {HIV-1} {PCR} amplification. Three samples showed a nucleotide divergence compatible with a {non-B} subtype classification. The phylogenetic analysis, performed on both {HIV-1} env and gag regions, confirms the molecular sub-typing prediction, given that 1 sample falls into the C subtype and 2 into the G subtype. The B subtype isolates show high levels of intra-subtype nucleotide divergence, compatible with a long-lasting epidemic and a progressive {HIV-1} molecular {diversification.CONCLUSION:The} Italian {HIV-1} epidemic is still mostly attributable to the B subtype, regardless the transmission route, which shows an increasing nucleotide heterogeneity. Heterosexual transmission and the interracial blending, however, are slowly introducing novel {HIV-1} subtypes. Therefore, a molecular monitoring is needed to follow the constant evolution of the {HIV-1} epidemic.},  Author = {Buonaguro, Luigi and Petrizzo, Annacarmen and Tagliamonte, Maria and Vitone, Francesca and Re, Maria and Pilotti, Elisabetta and Casoli, Claudio and Sbreglia, Costanza and Perrella, Oreste and Tornesello, Maria and Buonaguro, Franco},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Infectious Agents and Cancer},  Number = {1},  Pages = {13},  Title = {Molecular and phylogenetic analysis of {HIV-1} variants circulating in Italy},  Url = {http://www.infectagentscancer.com/content/3/1/13},  Volume = {3},  Year = {2008},  Bdsk-Url-1 = {http://www.infectagentscancer.com/content/3/1/13}}  @book{burnham:2002mo,  Author = {Burnham, K.P. and Anderson, D.R.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Isbn = {0387953647},  Publisher = {Springer Verlag},  Title = {{Model selection and multimodel inference: a practical information-theoretic approach}},  Year = {2002}}  @article{Bush:1999vn,  Abstract = {Eighteen codons in the HA1 domain of the hemagglutinin genes of human influenza A subtype H3 appear to be under positive selection to change the amino acid they encode. Retrospective tests show that viral lineages undergoing the greatest number of mutations in the positively selected codons were the progenitors of future H3 lineages in 9 of 11 recent influenza seasons. Codons under positive selection were associated with antibody combining site A or B or the sialic acid receptor binding site. However, not all codons in these sites had predictive value. Monitoring new H3 isolates for additional changes in positively selected codons might help identify the most fit extant viral strains that arise during antigenic drift.},  Author = {Bush, R M and Bender, C A and Subbarao, K and Cox, N J and Fitch, W M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Amino Acid Substitution; Antigenic Variation; Binding Sites; Codon; Epitopes; Evolution, Molecular; Forecasting; Genes, Viral; Hemagglutinin Glycoproteins, Influenza Virus; Humans; Influenza A virus; Influenza, Human; Mutation; Phylogeny; Probability; Protein Structure, Tertiary; Receptors, Cell Surface; Retrospective Studies; Selection, Genetic},  Month = {Dec},  Number = {5446},  Pages = {1921-5},  Pmid = {10583948},  Pst = {ppublish},  Title = {Predicting the evolution of human influenza A},  Volume = {286},  Year = {1999}}  @article{Cartwright:2011uq,  Abstract = {Although most of the important evolutionary events in the history of biology can only be studied via interspecific comparisons, it is challenging to apply the rich body of population genetic theory to the study of interspecific genetic variation. Probabilistic modeling of the substitution process would ideally be derived from first principles of population genetics, allowing a quantitative connection to be made between the parameters describing mutation, selection, drift, and the patterns of interspecific variation. There has been progress in reconciling population genetics and interspecific evolution for the case where mutation rates are sufficiently low, but when mutation rates are higher, reconciliation has been hampered due to complications from how the loss or fixation of new mutations can be influenced by linked nonneutral polymorphisms (i.e., the Hill-Robertson effect). To investigate the generation of interspecific genetic variation when concurrent fitness-affecting polymorphisms are common and the Hill-Robertson effect is thereby potentially strong, we used the Wright-Fisher model of population genetics to simulate very many generations of mutation, natural selection, and genetic drift. This was done so that the chronological history of advantageous, deleterious, and neutral substitutions could be traced over time along the ancestral lineage. Our simulations show that the process by which a nonrecombining sequence changes over time can markedly deviate from the Markov assumption that is ubiquitous in molecular phylogenetics. In particular, we find tendencies for advantageous substitutions to be followed by deleterious ones and for deleterious substitutions to be followed by advantageous ones. Such non-Markovian patterns reflect the fact that the fate of the ancestral lineage depends not only on its current allelic state but also on gene copies not belonging to the ancestral lineage. Although our simulations describe nonrecombining sequences, we conclude by discussing how non-Markovian behavior of the ancestral lineage is plausible even when recombination rates are not low. As a result, we believe that increased attention needs to be devoted to the robustness of evolutionary inference procedures that rely upon the Markov assumption.},  Author = {Cartwright, Reed A and Lartillot, Nicolas and Thorne, Jeffrey L},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/sysbio/syr012},  Journal = {Syst Biol},  Journal-Full = {Systematic biology},  Month = {Mar},  Pages = {doi:10.1093/sysbio/syr012},  Pmid = {21398626},  Pst = {aheadofprint},  Title = {History Can Matter: Non-Markovian Behavior of Ancestral Lineages},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/sysbio/syr012}}  @article{Champagnat:2007kx,  Abstract = {The biological theory of adaptive dynamics proposes a description of the long-term evolution of a structured asexual population. It is based on the assumptions of large population, rare mutations and small mutation steps, that lead to a deterministic ODE describing the evolution of the dominant type, called the "canonical equation of adaptive dynamics." Here, in order to include the effect of stochasticity (genetic drift), we consider self-regulated randomly fluctuating populations subject to mutation, so that the number of coexisting types may fluctuate. We apply a limit of rare mutations to these populations, while keeping the population size finite. This leads to a jump process, the so-called "trait substitution sequence," where evolution proceeds by successive invasions and fixations of mutant types. Then we apply a limit of small mutation steps (weak selection) to this jump process, that leads to a diffusion process that we call the "canonical diffusion of adaptive dynamics," in which genetic drift is combined with directional selection driven by the gradient of the fixation probability, also interpreted as an invasion fitness. Finally, we study in detail the particular case of multitype logistic branching populations and seek explicit formulae for the invasion fitness of a mutant deviating slightly from the resident type. In particular, second-order terms of the fixation probability are products of functions of the initial mutant frequency, times functions of the initial total population size, called the invasibility coefficients of the resident by increased fertility, defence, aggressiveness, isolation or survival.},  Address = {PO BOX 22718, BEACHWOOD, OH 44122 USA},  Author = {Champagnat, Nicolas and Lambert, Amaury},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {DOI 10.1214/105051606000000628},  Isi = {000244850700005},  Isi-Recid = {155092887},  Isi-Ref-Recids = {34183189 16214003 151802802 146048521 149981180 20062755 110943913 124791420 96162330 62459663 150488832 32444680 137459736 14731497 115416250 102791328 92783578 64301968 50517071 92403644 12388006 146048497 150391628 144299841 29560225 81735832 27948158 79787280 99596891 111053790 146048511},  Journal = {Annals of Applied Probability},  Keywords = {logistic branching process; multitype birth death competition process; population dynamics; density-dependence; competition; fixation probability; genetic drift; weak selection; adaptive dynamics; invasion fitness; timescale separation; trait substitution sequence; diffusion approximation; harmonic equations; convergence of measure-valued processes},  Month = feb,  Number = {1},  Pages = {102--155},  Publisher = {INST MATHEMATICAL STATISTICS},  Times-Cited = {7},  Title = {Evolution of discrete populations and the canonical diffusion of adaptive dynamics},  Volume = {17},  Year = {2007},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=000244850700005}}  @article{chen:1997hu,  Author = {Chen, Z and Luckay, A and Sodora, {DL} and Telfer, P and Reed, P and Gettie, A and Kanu, {JM} and Sadek, {RF} and Yee, J and Ho, {DD} and Zhang, L and Marx, {PA}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {The Journal of Virology},  Month = may,  Number = {5},  Pages = {3953--3960},  Title = {Human immunodeficiency virus type 2 {(HIV-2)} seroprevalence and characterization of a distinct {HIV-2} genetic subtype from the natural range of simian immunodeficiency virus-infected sooty mangabeys},  Url = {http://jvi.asm.org/cgi/content/abstract/71/5/3953},  Volume = {71},  Year = {1997},  Bdsk-Url-1 = {http://jvi.asm.org/cgi/content/abstract/71/5/3953}}  @article{Chen:2005uq,  Abstract = {The objectives of this paper to analyse, model and simulate the spread of an infectious disease by resorting to modern stochastic algorithms. The approach renders it possible to circumvent the simplifying assumption of linearity imposed in the majority of the past works on stochastic analysis of epidemic processes. Infectious diseases are often transmitted through contacts of those infected with those susceptible; hence the processes are inherently nonlinear. According to the classical model of Kermack and McKendrick, or the SIR model, three classes of populations are involved in two types of processes: conversion of susceptibles (S) to infectives (I) and conversion of infectives to removed (R). The master equations of the SIR process have been formulated through the probabilistic population balance around a particular state by considering the mutually exclusive events. The efficacy of the present methodology is mainly attributable to its ability to derive the governing equations for the means, variances and covariance of the random variables by the method of system-size expansion of the nonlinear master equations. Solving these equations simultaneously along with rates associated influenza epidemic data yields information concerning not only the means of the three populations but also the minimal uncertainties of these populations inherent in the epidemic. The stochastic pathways of the three different classes of populations during an epidemic, i.e. their means and the fluctuations around these means, have also been numerically simulated independently by the algorithm derived from the master equations, as well as by an event-driven Monte Carlo algorithm. The master equation and Monte Carlo algorithms have given rise to the identical results.},  Author = {Chen, Wei-Yin and Bokka, Sankar},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.jtbi.2004.11.033},  Journal = {J Theor Biol},  Journal-Full = {Journal of theoretical biology},  Mesh = {Algorithms; Communicable Diseases; Disease Outbreaks; Disease Susceptibility; Humans; Models, Biological; Models, Statistical; Monte Carlo Method; Probability},  Month = {Jun},  Number = {4},  Pages = {455-70},  Pmid = {15808867},  Pst = {ppublish},  Title = {Stochastic modeling of nonlinear epidemiology},  Volume = {234},  Year = {2005},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jtbi.2004.11.033}}  @article{chen:2006av,  Author = {Chen, R. and Holmes, E. C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msl102},  Issn = {0737-4038},  Journal = {Molecular Biology and Evolution},  Number = {12},  Pages = {2336--2341},  Title = {Avian Influenza Virus Exhibits Rapid Evolutionary Dynamics},  Url = {http://mbe.oxfordjournals.org/cgi/doi/10.1093/molbev/msl102},  Volume = {23},  Year = {2006},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/doi/10.1093/molbev/msl102},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/msl102}}  @article{chen:2006es,  Author = {Chen, H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1073/pnas.0511120103},  Issn = {0027-8424},  Journal = {Proceedings of the National Academy of Sciences},  Number = {8},  Pages = {2845--2850},  Title = {Establishment of multiple sublineages of {H5N1} influenza virus in Asia: Implications for pandemic control},  Url = {http://www.pnas.org/cgi/doi/10.1073/pnas.0511120103},  Volume = {103},  Year = {2006},  Bdsk-Url-1 = {http://www.pnas.org/cgi/doi/10.1073/pnas.0511120103},  Bdsk-Url-2 = {http://dx.doi.org/10.1073/pnas.0511120103}}  @article{claas:1998hu,  Abstract = {{BACKGROUND:} In May, 1997, a 3-year-old boy in Hong Kong was admitted to the hospital and subsequently died from influenza pneumonia, acute respiratory distress syndrome, Reye's syndrome, multiorgan failure, and disseminated intravascular coagulation. An influenza A {H5N1} virus was isolated from a tracheal aspirate of the boy. Preceding this incident, avian influenza outbreaks of high mortality were reported from three chicken farms in Hong Kong, and the virus involved was also found to be of the H5 subtype. {METHODS:} We carried out an antigenic and molecular comparison of the influenza A {H5N1} virus isolated from the boy with one of the viruses isolated from outbreaks of avian influenza by haemagglutination-inhibition and neuraminidase-inhibition assays and nucleotide sequence analysis. {FINDINGS:} Differences were observed in the antigenic reactivities of the viruses by the haemagglutination-inhibition assay. However, nucleotide sequence analysis of all gene segments revealed that the human virus {A/Hong} Kong/156/97 was genetically closely related to the avian {A/chicken/Hong} Kong/258/97. {INTERPRETATION:} Although direct contact between the sick child and affected chickens has not been established, our results suggest transmission of the virus from infected chickens to the child without another intermediate mammalian host acting as a "mixing vessel". This event illustrates the importance of intensive global influenza surveillance.},  Author = {Claas, E C and Osterhaus, A D and van Beek, R and Jong, J C De and Rimmelzwaan, G F and Senne, D A and Krauss, S and Shortridge, K F and Webster, R G},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/S0140-6736(97)11212-0},  Issn = {0140-6736},  Journal = {Lancet},  Keywords = {Amino Acid Sequence, Animals, Base Sequence, Chickens, Child, Preschool, Disease Outbreaks, Hong Kong, Humans, Influenza A virus, Influenza A Virus, {H5N1} Subtype, Influenza in Birds, Influenza, Human, Male, Molecular Sequence Data},  Month = feb,  Note = {{PMID:} 9482438},  Number = {9101},  Pages = {472--477},  Title = {Human influenza A {H5N1} virus related to a highly pathogenic avian influenza virus},  Url = {http://www.ncbi.nlm.nih.gov/pubmed/9482438},  Volume = {351},  Year = {1998},  Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed/9482438},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/S0140-6736(97)11212-0}}  @article{Coelho:2008uq,  Abstract = {The construction of complex spatial simulation models such as those used in network epidemiology, is a daunting task due to the large amount of data involved in their parameterization. Such data, which frequently resides on large geo-referenced databases, has to be processed and assigned to the various components of the model. All this just to construct the model, then it still has to be simulated and analyzed under different epidemiological scenarios. This workflow can only be achieved efficiently by computational tools that can automate most, if not all, these time-consuming tasks. In this paper, we present a simulation software, Epigrass, aimed to help designing and simulating network-epidemic models with any kind of node behavior.},  Author = {Coelho, Fl{\'a}vio C and Cruz, Oswaldo G and Code{\c c}o, Cl{\'a}udia T},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1186/1751-0473-3-3},  Journal = {Source Code Biol Med},  Journal-Full = {Source code for biology and medicine},  Pages = {3},  Pmc = {PMC2275240},  Pmid = {18302744},  Pst = {epublish},  Title = {Epigrass: a tool to study disease spread in complex networks},  Volume = {3},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1751-0473-3-3}}  @article{Coffin:1995vn,  Abstract = {Several recent reports indicate that the long, clinically latent phase that characterizes human immunodeficiency virus (HIV) infection of humans is not a period of viral inactivity, but an active process in which cells are being infected and dying at a high rate and in large numbers. These results lead to a simple steady-state model in which infection, cell death, and cell replacement are in balance, and imply that the unique feature of HIV is the extraordinarily large number of replication cycles that occur during infection of a single individual. This turnover drives both the pathogenic process and (even more than mutation rate) the development of genetic variation. This variation includes the inevitable and, in principle, predictable accumulation of mutations such as those conferring resistance to antiviral drugs whose presence before therapy must be considered in the design of therapeutic strategies.},  Author = {Coffin, J M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Acquired Immunodeficiency Syndrome; Antiviral Agents; CD4 Lymphocyte Count; CD4-Positive T-Lymphocytes; Cell Death; DNA, Viral; Drug Resistance, Microbial; Genetic Variation; HIV; HIV Infections; Humans; Kinetics; Mutation; Proviruses; RNA, Viral; Viremia; Virus Replication},  Month = {Jan},  Number = {5197},  Pages = {483-9},  Pmid = {7824947},  Pst = {ppublish},  Title = {HIV population dynamics in vivo: implications for genetic variation, pathogenesis, and therapy},  Volume = {267},  Year = {1995}}  @article{Colizza:2006kx,  Abstract = {The global spread of emergent diseases is inevitably entangled with the structure of the population flows among different geographical regions. The airline transportation network in particular shrinks the geographical space by reducing travel time between the world's most populated areas and defines the main channels along which emergent diseases will spread. In this paper, we investigate the role of the large-scale properties of the airline transportation network in determining the global propagation pattern of emerging diseases. We put forward a stochastic computational framework for the modeling of the global spreading of infectious diseases that takes advantage of the complete International Air Transport Association 2002 database complemented with census population data. The model is analyzed by using for the first time an information theory approach that allows the quantitative characterization of the heterogeneity level and the predictability of the spreading pattern in presence of stochastic fluctuations. In particular we are able to assess the reliability of numerical forecast with respect to the intrinsic stochastic nature of the disease transmission and travel flows. The epidemic pattern predictability is quantitatively determined and traced back to the occurrence of epidemic pathways defining a backbone of dominant connections for the disease spreading. The presented results provide a general computational framework for the analysis of containment policies and risk forecast of global epidemic outbreaks.},  Author = {Colizza, V and Barrat, A and Barth{\'e}lemy, M and Vespignani, A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1007/s11538-006-9077-9},  Journal = {Bull Math Biol},  Journal-Full = {Bulletin of mathematical biology},  Mesh = {Communicable Diseases; Disease Outbreaks; Humans; Models, Biological; Stochastic Processes; Travel},  Month = {Nov},  Number = {8},  Pages = {1893-921},  Pmid = {17086489},  Pst = {ppublish},  Title = {The modeling of global epidemics: stochastic dynamics and predictability},  Volume = {68},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1007/s11538-006-9077-9}}  @article{Cottam:2008zr,  Abstract = {Estimating detailed transmission trees that reflect the relationships between infected individuals or populations during a disease outbreak often provides valuable insights into both the nature of disease transmission and the overall dynamics of the underlying epidemiological process. These trees may be based on epidemiological data that relate to the timing of infection and infectiousness, or genetic data that show the genetic relatedness of pathogens isolated from infected individuals. Genetic data are becoming increasingly important in the estimation of transmission trees of viral pathogens due to their inherently high mutation rate. Here, we propose a maximum-likelihood approach that allows epidemiological and genetic data to be combined within the same analysis to infer probable transmission trees. We apply this approach to data from 20 farms infected during the 2001 UK foot-and-mouth disease outbreak, using complete viral genome sequences from each infected farm and information on when farms were first estimated to have developed clinical disease and when livestock on these farms were culled. Incorporating known infection links due to animal movement prior to imposition of the national movement ban results in the reduction of the number of trees from 41472 that are consistent with the genetic data to 1728, of which just 4 represent more than 95\% of the total likelihood calculated using a model that accounts for the epidemiological data. These trees differ in several ways from those constructed prior to the availability of genetic data.},  Author = {Cottam, Eleanor M and Th{\'e}baud, Ga{\"e}l and Wadsworth, Jemma and Gloster, John and Mansley, Leonard and Paton, David J and King, Donald P and Haydon, Daniel T},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1098/rspb.2007.1442},  Journal = {Proc Biol Sci},  Journal-Full = {Proceedings. Biological sciences / The Royal Society},  Mesh = {Agriculture; Animals; Base Sequence; Disease Outbreaks; England; Foot-and-Mouth Disease; Foot-and-Mouth Disease Virus; Likelihood Functions; Monte Carlo Method; Time Factors},  Month = {Apr},  Number = {1637},  Pages = {887-95},  Pmc = {PMC2599933},  Pmid = {18230598},  Pst = {ppublish},  Title = {Integrating genetic and epidemiological data to determine transmission pathways of foot-and-mouth disease virus},  Volume = {275},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rspb.2007.1442}}  @article{cutler:2000es,  Author = {Cutler, D.J.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0737-4038},  Journal = {Molecular Biology and Evolution},  Number = {11},  Pages = {1647},  Publisher = {SMBE},  Title = {{Estimating divergence times in the presence of an overdispersed molecular clock}},  Volume = {17},  Year = {2000}}  @article{Day:2007dq,  Abstract = {Much of the existing theory for the evolutionary biology of infectious diseases uses an invasion analysis approach. In this Ideas and Perspectives article, we suggest that techniques from theoretical population genetics can also be profitably used to study the evolutionary epidemiology of infectious diseases. We highlight four ways in which population-genetic models provide benefits beyond those provided by most invasion analyses: (i) they can make predictions about the rate of pathogen evolution; (ii) they explicitly draw out the mechanistic way in which the epidemiological dynamics feed into evolutionary change, and thereby provide new insights into pathogen evolution; (iii) they can make predictions about the evolutionary consequences of non-equilibrium epidemiological dynamics; (iv) they can readily incorporate the effects of multiple host dynamics, and thereby account for phenomena such as immunological history and/or host co-evolution.},  Author = {Day, Troy and Gandon, Sylvain},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1461-0248.2007.01091.x},  Journal = {Ecol Lett},  Journal-Full = {Ecology letters},  Mesh = {Communicable Diseases; Evolution; Genetics, Population; Humans; Models, Genetic},  Month = {Oct},  Number = {10},  Pages = {876-88},  Pmid = {17845288},  Pst = {ppublish},  Title = {Applying population-genetic models in theoretical evolutionary epidemiology},  Volume = {10},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1461-0248.2007.01091.x}}  @article{Diekmann:1990ly,  Address = {175 FIFTH AVE, NEW YORK, NY 10010},  Author = {Diekmann, O and Heesterbeek, JAP and Metz, JAJ},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Isi = {A1990DG35000001},  Isi-Recid = {72556130},  Isi-Ref-Recids = {70416654 49486451 33835415 70416649 56019283 56144416 63162478 64838165 63076177 66692748 68010418 52586406 67319961 21203983 41700041 26543911 6965322},  Journal = {Journal of Mathematical Biology},  Number = {4},  Pages = {365-382},  Publisher = {Springer Verlag},  Times-Cited = {544},  Title = {On the Definition and the Computation of the Basic Reproduction Ratio R0 in Models for Infectious-Diseases in Heterogeneous Populations},  Volume = {28},  Year = {1990},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=A1990DG35000001}}  @article{Drummond:2005nx,  Abstract = {We introduce the Bayesian skyline plot, a new method for estimating past population dynamics through time from a sample of molecular sequences without dependence on a prespecified parametric model of demographic history. We describe a Markov chain Monte Carlo sampling procedure that efficiently samples a variant of the generalized skyline plot, given sequence data, and combines these plots to generate a posterior distribution of effective population size through time. We apply the Bayesian skyline plot to simulated data sets and show that it correctly reconstructs demographic history under canonical scenarios. Finally, we compare the Bayesian skyline plot model to previous coalescent approaches by analyzing two real data sets (hepatitis C virus in Egypt and mitochondrial DNA of Beringian bison) that have been previously investigated using alternative coalescent methods. In the bison analysis, we detect a severe but previously unrecognized bottleneck, estimated to have occurred 10,000 radiocarbon years ago, which coincides with both the earliest undisputed record of large numbers of humans in Alaska and the megafaunal extinctions in North America at the beginning of the Holocene.},  Author = {Drummond, A J and Rambaut, A and Shapiro, B and Pybus, O G},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:53:16 +0000},  Doi = {10.1093/molbev/msi103},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Algorithms; Animals; Bayes Theorem; Bison; DNA, Mitochondrial; Egypt; Evolution, Molecular; Genetics, Population; Hepacivirus; Hepatitis C; Humans; Markov Chains; Models, Genetic; Monte Carlo Method; Population Density; Population Dynamics; Time Factors},  Month = {5},  Number = {5},  Pages = {1185-92},  Pmid = {15703244},  Pst = {ppublish},  Title = {Bayesian coalescent inference of past population dynamics from molecular sequences},  Volume = {22},  Year = {2005},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msi103}}  @article{Drummond:2006dq,  Abstract = {In phylogenetics, the unrooted model of phylogeny and the strict molecular clock model are two extremes of a continuum. Despite their dominance in phylogenetic inference, it is evident that both are biologically unrealistic and that the real evolutionary process lies between these two extremes. Fortunately, intermediate models employing relaxed molecular clocks have been described. These models open the gate to a new field of "relaxed phylogenetics." Here we introduce a new approach to performing relaxed phylogenetic analysis. We describe how it can be used to estimate phylogenies and divergence times in the face of uncertainty in evolutionary rates and calibration times. Our approach also provides a means for measuring the clocklikeness of datasets and comparing this measure between different genes and phylogenies. We find no significant rate autocorrelation among branches in three large datasets, suggesting that autocorrelated models are not necessarily suitable for these data. In addition, we place these datasets on the continuum of clocklikeness between a strict molecular clock and the alternative unrooted extreme. Finally, we present analyses of 102 bacterial, 106 yeast, 61 plant, 99 metazoan, and 500 primate alignments. From these we conclude that our method is phylogenetically more accurate and precise than the traditional unrooted model while adding the ability to infer a timescale to evolution.},  Author = {Drummond, Alexei J and Ho, Simon Y W and Phillips, Matthew J and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pbio.0040088},  Journal = {PLoS Biol},  Journal-Full = {PLoS biology},  Mesh = {Animals; Bacteria; Bayes Theorem; Computer Simulation; Dengue Virus; Evolution; Fishes; Fungi; Genetic Variation; Influenza A virus; Insects; Markov Chains; Marsupialia; Models, Biological; Monte Carlo Method; Phylogeny; Plants; Primates; Time Factors},  Month = {May},  Number = {5},  Pages = {e88},  Pmc = {PMC1395354},  Pmid = {16683862},  Pst = {ppublish},  Title = {Relaxed phylogenetics and dating with confidence},  Volume = {4},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pbio.0040088}}  @article{Drummond2007,  Abstract = {BACKGROUND: The evolutionary analysis of molecular sequence variation is a statistical enterprise. This is reflected in the increased use of probabilistic models for phylogenetic inference, multiple sequence alignment, and molecular population genetics. Here we present BEAST: a fast, flexible software architecture for Bayesian analysis of molecular sequences related by an evolutionary tree. A large number of popular stochastic models of sequence evolution are provided and tree-based models suitable for both within- and between-species sequence data are implemented. RESULTS: BEAST version 1.4.6 consists of 81000 lines of Java source code, 779 classes and 81 packages. It provides models for DNA and protein sequence evolution, highly parametric coalescent analysis, relaxed clock phylogenetics, non-contemporaneous sequence data, statistical alignment and a wide range of options for prior distributions. BEAST source code is object-oriented, modular in design and freely available at http://beast-mcmc.googlecode.com/ under the GNU LGPL license. CONCLUSION: BEAST is a powerful and flexible evolutionary analysis package for molecular sequence variation. It also provides a resource for the further development of new models and statistical methods of evolutionary analysis.},  Author = {Drummond, Alexei J and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2013-05-09 22:27:31 +1200},  Doi = {10.1186/1471-2148-7-214},  Journal = {BMC Evol Biol},  Journal-Full = {BMC evolutionary biology},  Mesh = {Bayes Theorem; Computational Biology; Computer Simulation; Evolution, Molecular; Models, Genetic; Models, Statistical; Phylogeny; Sequence Analysis, DNA; Software},  Pages = {214},  Pmc = {PMC2247476},  Pmid = {17996036},  Pst = {epublish},  Title = {BEAST: Bayesian evolutionary analysis by sampling trees},  Volume = {7},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2148-7-214}}  @article{Drummond2008,  Abstract = {BACKGROUND: Many data summary statistics have been developed to detect departures from neutral expectations of evolutionary models. However questions about the neutrality of the evolution of genetic loci within natural populations remain difficult to assess. One critical cause of this difficulty is that most methods for testing neutrality make simplifying assumptions simultaneously about the mutational model and the population size model. Consequentially, rejecting the null hypothesis of neutrality under these methods could result from violations of either or both assumptions, making interpretation troublesome. RESULTS: Here we harness posterior predictive simulation to exploit summary statistics of both the data and model parameters to test the goodness-of-fit of standard models of evolution. We apply the method to test the selective neutrality of molecular evolution in non-recombining gene genealogies and we demonstrate the utility of our method on four real data sets, identifying significant departures of neutrality in human influenza A virus, even after controlling for variation in population size. CONCLUSION: Importantly, by employing a full model-based Bayesian analysis, our method separates the effects of demography from the effects of selection. The method also allows multiple summary statistics to be used in concert, thus potentially increasing sensitivity. Furthermore, our method remains useful in situations where analytical expectations and variances of summary statistics are not available. This aspect has great potential for the analysis of temporally spaced data, an expanding area previously ignored for limited availability of theory and methods.},  Author = {Drummond, Alexei J and Suchard, Marc A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-20 23:32:48 +0000},  Doi = {10.1186/1471-2156-9-68},  Journal = {BMC Genetics},  Journal-Full = {BMC genetics},  Mesh = {Animals; Bayes Theorem; Computer Simulation; Evolution, Molecular; Genetics, Population; Models, Genetic; Models, Statistical; RNA Viruses; Ursidae},  Pages = {68},  Pmc = {PMC2645432},  Pmid = {18976476},  Pst = {epublish},  Title = {Fully Bayesian tests of neutrality using genealogical summary statistics},  Volume = {9},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2156-9-68}}  @article{drummond:2010ba,  Author = {Drummond, A. J. and Suchard, M. A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 00:52:58 +0000},  Issn = {1741-7007},  Journal = {BMC biology},  Number = {1},  Pages = {114},  Publisher = {BioMed Central Ltd},  Title = {{Bayesian random local clocks, or one rate to rule them all}},  Volume = {8},  Year = {2010}}  @article{Drummond:2010fk,  Abstract = {Systems evolving under the influence of autocatalytic processes have been the subject of much study due to their appearance in a wide variety of contexts. Well known examples range from the simplest autocatalytic chemical reactions, biochemical models of ribozyme or prion replication, right up to the duplication of entire organisms in models of population dynamics. While the deterministic approach frequently taken to model such systems is adequate in the limit of large reactant numbers, the intrinsic fluctuations exert an important influence on the dynamics when the supply of reactants is limited. In particular, when combined with spontaneous degradation of the autocatalytic reactant population, such fluctuations can lead to the extinction of that population. In this paper, we study reversible autocatalytic processes of the form X + Y reversible arrow 2X in the limit that there exists a surplus of Y and in the presence of a spontaneous degradation process X -> Z. Through the use of the Poisson representation, we identify an exact analytical expression for the mean extinction time of the X population. We show that the exact result can be neatly approximated by an Arrhenius-like expression involving an effective activation energy separating a quasi-stationary state from the extinct state.},  Address = {1155 16TH ST, NW, WASHINGTON, DC 20036 USA},  Author = {Drummond, Peter D. and Vaughan, Timothy G. and Drummond, Alexei J.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {DOI 10.1021/jp104471e},  Isi = {000282210000002},  Isi-Recid = {191933250},  Isi-Ref-Recids = {160062474 35006563 160920273 611690 191933251 98526560 2943055 137263911 32932953 96069854 33073076 30909561 127154082 183537701 183537700 125184029 6566 96900539 180436335 159828079 191933252 174041446 191933253 153401370 147647895 127825 120575784 133389973 126777099 142120143 157336336 118713804 156016467 133138071 93936160 157678948 7007221 1203123 143185316 137632795},  Journal = {Journal of Physical Chemistry a},  Month = oct,  Number = {39},  Pages = {10481--10491},  Publisher = {AMER CHEMICAL SOC},  Times-Cited = {1},  Title = {Extinction Times in Autocatalytic Systems},  Volume = {114},  Year = {2010},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=000282210000002}}  @incollection{drummondNRS:2003,  Author = {Drummond, Alexei J. and Nicholls, Geoff K. and Rodrigo, A. G. and Solomon, Wiremu},  Booktitle = {Tools for Constructing Chronologies: crossing disciplinary boundaries},  Chapter = {7},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 01:01:25 +0000},  Editor = {Buck, C E. and Millard, A R.},  Pages = {149-174},  Publisher = {Springer},  Series = {Lecture Notes in Statistics},  Title = {Genealogies from time-stamped sequence data},  Volume = {177},  Year = {2003}}  @article{dugan:2008ev,  Abstract = {We surveyed the genetic diversity among avian influenza virus {(AIV)} in wild birds, comprising 167 complete viral genomes from 14 bird species sampled in four locations across the United States. These isolates represented 29 type A influenza virus hemagglutinin {(HA)} and neuraminidase {(NA)} subtype combinations, with up to 26\% of isolates showing evidence of mixed subtype infection. Through a phylogenetic analysis of the largest data set of {AIV} genomes compiled to date, we were able to document a remarkably high rate of genome reassortment, with no clear pattern of gene segment association and occasional inter-hemisphere gene segment migration and reassortment. From this, we propose that {AIV} in wild birds forms transient "genome constellations," continually reshuffled by reassortment, in contrast to the spread of a limited number of stable genome constellations that characterizes the evolution of mammalian-adapted influenza A viruses.},  Author = {Dugan, Vivien G and Chen, Rubing and Spiro, David J and Sengamalay, Naomi and Zaborsky, Jennifer and Ghedin, Elodie and Nolting, Jacqueline and Swayne, David E and Runstadler, Jonathan A and Happ, George M and Senne, Dennis A and Wang, Ruixue and Slemons, Richard D and Holmes, Edward C and Taubenberger, Jeffery K},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.ppat.1000076},  Issn = {1553-7374},  Journal = {{PLoS} Pathogens},  Keywords = {Animals, Animals, Wild, Birds, Cluster Analysis, {DNA,} Viral, Evolution, Molecular, Genetic Variation, Genome, Viral, Hemagglutinins, Viral, Influenza A virus, Influenza in Birds, Neuraminidase, Oligonucleotide Array Sequence Analysis, Phylogeny, Reassortant Viruses, United States},  Month = may,  Note = {{PMID:} 18516303},  Number = {5},  Pages = {e1000076},  Title = {The evolutionary genetics and emergence of avian influenza viruses in wild birds},  Url = {http://www.ncbi.nlm.nih.gov/pubmed/18516303},  Volume = {4},  Year = {2008},  Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed/18516303},  Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.ppat.1000076}}  @article{dunham:2009di,  Abstract = {In 1979, a lineage of avian-like {H1N1} influenza A viruses emerged in European swine populations independently from the classical swine {H1N1} virus lineage that had circulated in pigs since the Spanish influenza pandemic of 1918. To determine whether these two distinct lineages of swine-adapted {A/H1N1} viruses evolved from avian-like {A/H1N1} ancestors in similar ways, as might be expected given their common host species and origin, we compared patterns of nucleotide and amino acid change in whole genome sequences of both groups. An analysis of nucleotide compositional bias across all eight genomic segments for the two swine lineages showed a clear lineage-specific bias, although a segment-specific effect was also apparent. As such, there appears to be only a relatively weak host-specific selection pressure. Strikingly, despite each lineage evolving in the same species of host for decades, amino acid analysis revealed little evidence of either parallel or convergent changes. These findings suggest that although adaptation due to evolutionary lineages can be distinguished, there are functional and structural constraints on all gene segments and that the evolutionary trajectory of each lineage of swine {A/H1N1} virus has a strong historical contingency. Thus, in the context of emergence of an influenza A virus strain via a host switch event, it is difficult to predict what specific polygenic changes are needed for mammalian adaptation.},  Author = {Dunham, Eleca J and Dugan, Vivien G and Kaser, Emilee K and Perkins, Sarah E and Brown, Ian H and Holmes, Edward C and Taubenberger, Jeffery K},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.02565-08},  Issn = {1098-5514},  Journal = {Journal of Virology},  Keywords = {Amino Acid Substitution, Animals, Birds, Europe, Evolution, Molecular, Genome, Viral, Influenza A Virus, {H1N1} Subtype, Mutation, Nucleotides, Phylogeny, Selection, Genetic, Sequence Analysis, {DNA,} Sequence Analysis, Protein, Swine},  Month = jun,  Note = {{PMID:} 19297491},  Number = {11},  Pages = {5485--5494},  Title = {Different evolutionary trajectories of European avian-like and classical swine {H1N1} influenza A viruses},  Url = {http://www.ncbi.nlm.nih.gov/pubmed/19297491},  Volume = {83},  Year = {2009},  Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed/19297491},  Bdsk-Url-2 = {http://dx.doi.org/10.1128/JVI.02565-08}}  @article{Durrett:1994,  Author = {Durrett, R and Levin, S},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Theoretical Population Biology},  Month = {Aug},  Title = {The importance of being discrete (and spatial)},  Year = {1994}}  @article{edwards:1965me,  Author = {Edwards, AWF and Cavalli-Sforza, LL},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0006-341X},  Journal = {Biometrics},  Pages = {362--375},  Publisher = {JSTOR},  Title = {{A method for cluster analysis}},  Year = {1965}}  @article{Edwards:2006bh,  Abstract = {BACKGROUND: Genetic diversity of the human immunodeficiency virus type 1 (HIV-1) population within an individual is lost during transmission to a new host. The demography of transmission is an important determinant of evolutionary dynamics, particularly the relative impact of natural selection and genetic drift immediately following HIV-1 infection. Despite this, the magnitude of this population bottleneck is unclear. RESULTS: We use coalescent methods to quantify the bottleneck in a single case of homosexual transmission and find that over 99\% of the env and gag diversity present in the donor is lost. This was consistent with the diversity present at seroconversion in nine other horizontally infected individuals. Furthermore, we estimated viral diversity at birth in 27 infants infected through vertical transmission and found there to be no difference between the two modes of transmission. CONCLUSION: Assuming the bottleneck at transmission is selectively neutral, such a severe reduction in genetic diversity has important implications for adaptation in HIV-1, since beneficial mutations have a reduced chance of transmission.},  Author = {Edwards, Charles T T and Holmes, Edward C and Wilson, Daniel J and Viscidi, Raphael P and Abrams, Elaine J and Phillips, Rodney E and Drummond, Alexei J},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1186/1471-2148-6-28},  Journal = {BMC Evol Biol},  Journal-Full = {BMC evolutionary biology},  Mesh = {Bayes Theorem; Disease Transmission, Infectious; Evolution, Molecular; Female; Genetic Variation; HIV Core Protein p24; HIV Envelope Protein gp120; HIV Infections; HIV-1; Homosexuality; Humans; Infant, Newborn; Infectious Disease Transmission, Vertical; Male; Models, Biological; Phylogeny; Time Factors},  Pages = {28},  Pmc = {PMC1444934},  Pmid = {16556318},  Pst = {epublish},  Title = {Population genetic estimation of the loss of genetic diversity during horizontal transmission of HIV-1},  Volume = {6},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2148-6-28}}  @article{Edwards:2006qf,  Abstract = {The evolution of the human immunodeficiency virus (HIV-1) during chronic infection involves the rapid, continuous turnover of genetic diversity. However, the role of natural selection, relative to random genetic drift, in governing this process is unclear. We tested a stochastic model of genetic drift using partial envelope sequences sampled longitudinally in 28 infected children. In each case the Bayesian posterior (empirical) distribution of coalescent genealogies was estimated using Markov chain Monte Carlo methods. Posterior predictive simulation was then used to generate a null distribution of genealogies assuming neutrality, with the null and empirical distributions compared using four genealogy-based summary statistics sensitive to nonneutral evolution. Because both null and empirical distributions were generated within a coalescent framework, we were able to explicitly account for the confounding influence of demography. From the distribution of corrected P-values across patients, we conclude that empirical genealogies are more asymmetric than expected if evolution is driven by mutation and genetic drift only, with an excess of low-frequency polymorphisms in the population. This indicates that although drift may still play an important role, natural selection has a strong influence on the evolution of HIV-1 envelope. A negative relationship between effective population size and substitution rate indicates that as the efficacy of selection increases, a smaller proportion of mutations approach fixation in the population. This suggests the presence of deleterious mutations. We therefore conclude that intrahost HIV-1 evolution in envelope is dominated by purifying selection against low-frequency deleterious mutations that do not reach fixation.},  Author = {Edwards, C T T and Holmes, E C and Pybus, O G and Wilson, D J and Viscidi, R P and Abrams, E J and Phillips, R E and Drummond, A J},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1534/genetics.105.052019},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Base Sequence; Bayes Theorem; Child; Chronic Disease; Computer Simulation; Evolution, Molecular; Gene Products, env; Genes, Viral; Genetic Drift; HIV Infections; HIV-1; Humans; Molecular Sequence Data; Monte Carlo Method; Mutation; Polymorphism, Genetic; Selection, Genetic; Stochastic Processes},  Month = {Nov},  Number = {3},  Pages = {1441-53},  Pmc = {PMC1667091},  Pmid = {16951087},  Pst = {ppublish},  Title = {Evolution of the human immunodeficiency virus envelope gene is dominated by purifying selection},  Volume = {174},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.105.052019}}  @article{engen1998demographic,  Author = {Engen, S. and {\O}., Bakke and Islam, A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Biometrics},  Number = {3},  Pages = {840--846},  Title = {Demographic and environmental stochasticity-concepts and definitions},  Volume = {54},  Year = {1998}}  @article{ewing:2004us,  Abstract = {We present a Bayesian statistical inference approach for simultaneously estimating mutation rate, population sizes, and migration rates in an island-structured population, using temporal and spatial sequence data. Markov chain Monte Carlo is used to collect samples from the posterior probability distribution. We demonstrate that this chain implementation successfully reaches equilibrium and recovers truth for simulated data. A real {HIV} {DNA} sequence data set with two demes, semen and blood, is used as an example to demonstrate the method by fitting asymmetric migration rates and different population sizes. This data set exhibits a bimodal joint posterior distribution, with modes favoring different preferred migration directions. This full data set was subsequently split temporally for further analysis. Qualitative behavior of one subset was similar to the bimodal distribution observed with the full data set. The temporally split data showed significant differences in the posterior distributions and estimates of parameter values over time.},  Author = {Ewing, Greg and Nicholls, Geoff and Rodrigo, Allen G.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 01:00:22 +0000},  Doi = {10.1534/genetics.104.030411},  Journal = {Genetics},  Month = dec,  Number = {4},  Pages = {2407--2420},  Title = {Using Temporally Spaced Sequences to Simultaneously Estimate Migration Rates, Mutation Rate and Population Sizes in Measurably Evolving Populations},  Volume = {168},  Year = {2004},  Bdsk-Url-1 = {http://www.genetics.org.ezproxy.auckland.ac.nz/cgi/content/abstract/168/4/2407},  Bdsk-Url-2 = {http://dx.doi.org/10.1534/genetics.104.030411}}  @article{ewing:2006co,  Abstract = {We expand a coalescent-based method that uses serially sampled genetic data from a subdivided population to incorporate changes to the number of demes and patterns of colonization. Often, when estimating population parameters or other parameters of interest from genetic data, the demographic structure and parameters are not constant over evolutionary time. In this paper, we develop a Bayesian Markov chain Monte Carlo method that allows for step changes in mutation, migration, and population sizes, as well as changing numbers of demes, where the times of these changes are also estimated. We show that in parameter ranges of interest, reliable estimates can often be obtained, including the historical times of parameter changes. However, posterior densities of migration rates can be quite diffuse and estimators somewhat biased, as reported by other authors.},  Author = {Ewing, Greg and Rodrigo, Allen G.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 01:02:17 +0000},  Doi = {10.1093/molbev/msj111},  Journal = {Molecular Biology and Evolution},  Month = may,  Number = {5},  Pages = {988--996},  Title = {{Coalescent-Based} Estimation of Population Parameters When the Number of Demes Changes Over Time},  Volume = {23},  Year = {2006},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/23/5/988},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/msj111}}  @article{ewing:2006es,  Abstract = {Using the structured serial coalescent with Bayesian {MCMC} and serial samples, we estimate population size when some demes are not sampled or are hidden, ie ghost demes. It is found that even with the presence of a ghost deme, accurate inference was possible if the parameters are estimated with the true model. However with an incorrect model, estimates were biased and can be positively misleading. We extend these results to the case where there are sequences from the ghost at the last time sample. This case can arise in {HIV} patients, when some tissue samples and viral sequences only become available after death. When some sequences from the ghost deme are available at the last sampling time, estimation bias is reduced and accurate estimation of parameters associated with the ghost deme is possible despite sampling bias. Migration rates for this case are also shown to be good estimates when migration values are low.},  Author = {Ewing, Greg and Rodrigo, Allen G.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 01:01:42 +0000},  Issn = {1176-9343},  Journal = {Evolutionary Bioinformatics},  Note = {{PMID:} 19455215 {PMCID:} 2674663},  Pages = {227--235},  Title = {Estimating Population Parameters using the Structured Serial Coalescent with Bayesian {MCMC} Inference when some Demes are Hidden},  Volume = {2},  Year = {2006}}  @article{felsenstein:1981ev,  Abstract = {Summary The application of maximum likelihood techniques to the estimation of evolutionary trees from nucleic acid sequence data is discussed. A computationally feasible method for finding such maximum likelihood estimates is developed, and a computer program is available. This method has advantages over the traditional parsimony algorithms, which can give misleading results if rates of evolution differ in different lineages. It also allows the testing of hypotheses about the constancy of evolutionary rates by likelihood ratio tests, and gives rough indication of the error of the estimate of the tree.},  Author = {Felsenstein, Joseph},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1007/BF01734359},  Journal = {Journal of Molecular Evolution},  Month = nov,  Number = {6},  Pages = {368--376},  Shorttitle = {Evolutionary trees from {DNA} sequences},  Title = {Evolutionary trees from {DNA} sequences: A maximum likelihood approach},  Url = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1007/BF01734359},  Volume = {17},  Year = {1981},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1007/BF01734359},  Bdsk-Url-2 = {http://dx.doi.org/10.1007/BF01734359}}  @article{felsenstein:1985,  Author = {Felsenstein, Joseph},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {The American Naturalist},  Keywords = {comparative method, phylogenetics},  Month = {Jan},  Number = {1},  Pages = {1-15},  Title = {Phylogenies and the Comparative Method},  Volume = {125},  Year = {1985}}  @article{Felsenstein:2006uq,  Abstract = {A computer simulation study has been made of the accuracy of estimates of Theta = 4Nemu from a sample from a single isolated population of finite size. The accuracies turn out to be well predicted by a formula developed by Fu and Li, who used optimistic assumptions. Their formulas are restated in terms of accuracy, defined here as the reciprocal of the squared coefficient of variation. This should be proportional to sample size when the entities sampled provide independent information. Using these formulas for accuracy, the sampling strategy for estimation of Theta can be investigated. Two models for cost have been used, a cost-per-base model and a cost-per-read model. The former would lead us to prefer to have a very large number of loci, each one base long. The latter, which is more realistic, causes us to prefer to have one read per locus and an optimum sample size which declines as costs of sampling organisms increase. For realistic values, the optimum sample size is 8 or fewer individuals. This is quite close to the results obtained by Pluzhnikov and Donnelly for a cost-per-base model, evaluating other estimators of Theta. It can be understood by considering that the resources spent collecting larger samples prevent us from considering more loci. An examination of the efficiency of Watterson's estimator of Theta was also made, and it was found to be reasonably efficient when the number of mutants per generation in the sequence in the whole population is less than 2.5.},  Author = {Felsenstein, Joseph},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msj079},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Genetic Variation; Genetics, Population; Humans; Likelihood Functions; Mathematics; Models, Genetic; Phylogeny},  Month = {Mar},  Number = {3},  Pages = {691-700},  Pmid = {16364968},  Pst = {ppublish},  Title = {Accuracy of coalescent likelihood estimates: do we need more sites, more sequences, or more loci?},  Volume = {23},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msj079}}  @article{Ferguson:2003fk,  Abstract = {In pandemic and epidemic forms, influenza causes substantial, sometimes catastrophic, morbidity and mortality. Intense selection from the host immune system drives antigenic change in influenza A and B, resulting in continuous replacement of circulating strains with new variants able to re-infect hosts immune to earlier types. This 'antigenic drift' often requires a new vaccine to be formulated before each annual epidemic. However, given the high transmissibility and mutation rate of influenza, the constancy of genetic diversity within lineages over time is paradoxical. Another enigma is the replacement of existing strains during a global pandemic caused by 'antigenic shift'--the introduction of a new avian influenza A subtype into the human population. Here we explore ecological and immunological factors underlying these patterns using a mathematical model capturing both realistic epidemiological dynamics and viral evolution at the sequence level. By matching model output to phylogenetic patterns seen in sequence data collected through global surveillance, we find that short-lived strain-transcending immunity is essential to restrict viral diversity in the host population and thus to explain key aspects of drift and shift dynamics.},  Author = {Ferguson, Neil M and Galvani, Alison P and Bush, Robin M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nature01509},  Journal = {Nature},  Journal-Full = {Nature},  Mesh = {Antigenic Variation; Ecology; Evolution, Molecular; Genetic Variation; Humans; Influenza A virus; Influenza B virus; Influenza, Human; Models, Biological; Phylogeny; Population Dynamics},  Month = {Mar},  Number = {6930},  Pages = {428-33},  Pmid = {12660783},  Pst = {ppublish},  Title = {Ecological and immunological determinants of influenza evolution},  Volume = {422},  Year = {2003},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature01509}}  @article{Ferguson:2005qf,  Abstract = {Highly pathogenic H5N1 influenza A viruses are now endemic in avian populations in Southeast Asia, and human cases continue to accumulate. Although currently incapable of sustained human-to-human transmission, H5N1 represents a serious pandemic threat owing to the risk of a mutation or reassortment generating a virus with increased transmissibility. Identifying public health interventions that might be able to halt a pandemic in its earliest stages is therefore a priority. Here we use a simulation model of influenza transmission in Southeast Asia to evaluate the potential effectiveness of targeted mass prophylactic use of antiviral drugs as a containment strategy. Other interventions aimed at reducing population contact rates are also examined as reinforcements to an antiviral-based containment policy. We show that elimination of a nascent pandemic may be feasible using a combination of geographically targeted prophylaxis and social distancing measures, if the basic reproduction number of the new virus is below 1.8. We predict that a stockpile of 3 million courses of antiviral drugs should be sufficient for elimination. Policy effectiveness depends critically on how quickly clinical cases are diagnosed and the speed with which antiviral drugs can be distributed.},  Author = {Ferguson, Neil M and Cummings, Derek A T and Cauchemez, Simon and Fraser, Christophe and Riley, Steven and Meeyai, Aronrag and Iamsirithaworn, Sopon and Burke, Donald S},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nature04017},  Journal = {Nature},  Journal-Full = {Nature},  Mesh = {Age Distribution; Animals; Antiviral Agents; Asia, Southeastern; Communicable Disease Control; Computer Simulation; Contact Tracing; Humans; Influenza A virus; Influenza, Human; Models, Biological; Mutation; Population Density; Probability; Quarantine; Reassortant Viruses; Sensitivity and Specificity; Thailand; Time Factors; Travel; Virus Replication; Virus Shedding},  Month = {Sep},  Number = {7056},  Pages = {209-14},  Pmid = {16079797},  Pst = {ppublish},  Title = {Strategies for containing an emerging influenza pandemic in Southeast Asia},  Volume = {437},  Year = {2005},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature04017}}  @article{firth:2010us,  Abstract = {Double-stranded (ds) {DNA} viruses are often described as evolving through long-term codivergent associations with their hosts, a pattern that is expected to be associated with low rates of nucleotide substitution. However, the hypothesis of codivergence between {dsDNA} viruses and their hosts has rarely been rigorously tested, even though the vast majority of nucleotide substitution rate estimates for {dsDNA} viruses are based upon this assumption. It is therefore important to estimate the evolutionary rates of {dsDNA} viruses independent of the assumption of host-virus codivergence. Here, we explore the use of temporally-structured sequence data within a Bayesian framework to estimate the evolutionary rates for seven human {dsDNA} viruses, including variola virus (the causative agent of smallpox) and herpes simplex virus-1. Our analyses reveal that while the variola virus genome is likely to evolve at a rate of approximately 1 x 10-5 substitutions/site/year, and hence approaching that of many {RNA} viruses, the evolutionary rates of many other {dsDNA} viruses remain problematic to estimate. Synthetic data sets were constructed to inform our interpretation of the substitution rates estimated for these {dsDNA} viruses and the analysis of these demonstrated that given a sequence data set of appropriate length and sampling depth, it is possible to use time-structured analyses to estimate the substitution rates of many {dsDNA} viruses independently from the assumption of host-virus codivergence. Finally, the discovery that some {dsDNA} viruses may evolve at rates approaching those of {RNA} viruses has important implications for our understanding of the long-term evolutionary history and emergence potential of this major group of viruses.},  Author = {Firth, Cadhla and Kitchen, Andrew and Shapiro, Beth and Suchard, Marc A. and Holmes, Edward C. and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msq088},  Journal = {Mol Biol Evol},  Month = apr,  Pages = {msq088},  Title = {Using {Time-Structured} Data to Estimate Evolutionary Rates of {Double-Stranded} {DNA} Viruses},  Url = {http://mbe.oxfordjournals.org.ezproxy.auckland.ac.nz/cgi/content/abstract/msq088v1},  Year = {2010},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org.ezproxy.auckland.ac.nz/cgi/content/abstract/msq088v1},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/msq088}}  @book{Fisher:1930ge,  Address = {Oxford},  Author = {Fisher, R.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Publisher = {Clarendon Press},  Title = {{Genetical Theory of Natural Selection}},  Year = {1930}}  @article{Fitch:1991ve,  Abstract = {We earlier suggested that type A human influenza virus genes undergo positive Darwinian selection through immune surveillance. This requires more favorable amino acid replacements fixed in antigenic sites among the surviving lineages than among the extinct lineages. We now show that viral hemagglutinins fix proportionately more amino acid replacements in antigenic sites in the trunk of the evolutionary tree (survivors) than in the branches (nonsurvivors), demonstrating that type A human influenza virus is undergoing positive Darwinian evolution. The hemagglutinin gene is evolving 3 times faster than the nonstructural gene and the average age of the sampled nonsurvivors is only 1.6 years, so that extinction is not only common but rapid.},  Author = {Fitch, W M and Leiter, J M and Li, X Q and Palese, P},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Amino Acid Sequence; Biological Evolution; Genes, Viral; Hemagglutinins, Viral; Influenza A virus; Molecular Sequence Data},  Month = {May},  Number = {10},  Pages = {4270-4},  Pmc = {PMC51640},  Pmid = {1840695},  Pst = {ppublish},  Title = {Positive Darwinian evolution in human influenza A viruses},  Volume = {88},  Year = {1991}}  @article{Fitch:1997qf,  Abstract = {We have studied the HA1 domain of 254 human influenza A(H3N2) virus genes for clues that might help identify characteristics of hemagglutinins (HAs) of circulating strains that are predictive of that strain's epidemic potential. Our preliminary findings include the following. (i) The most parsimonious tree found requires 1,260 substitutions of which 712 are silent and 548 are replacement substitutions. (ii) The HA1 portion of the HA gene is evolving at a rate of 5.7 nucleotide substitutions/year or 5.7 x 10(-3) substitutions/site per year. (iii) The replacement substitutions are distributed randomly across the three positions of the codon when allowance is made for the number of ways each codon can change the encoded amino acid. (iv) The replacement substitutions are not distributed randomly over the branches of the tree, there being 2.2 times more changes per tip branch than for non-tip branches. This result is independent of how the virus was amplified (egg grown or kidney cell grown) prior to sequencing or if sequencing was carried out directly on the original clinical specimen by PCR. (v) These excess changes on the tip branches are probably the result of a bias in the choice of strains to sequence and the detection of deleterious mutations that had not yet been removed by negative selection. (vi) There are six hypervariable codons accumulating replacement substitutions at an average rate that is 7.2 times that of the other varied codons. (vii) The number of variable codons in the trunk branches (the winners of the competitive race against the immune system) is 47 +/- 5, significantly fewer than in the twigs (90 +/- 7), which in turn is significantly fewer variable codons than in tip branches (175 +/- 8). (viii) A minimum of one of every 12 branches has nodes at opposite ends representing viruses that reside on different continents. This is, however, no more than would be expected if one were to randomly reassign the continent of origin of the isolates. (ix) Of 99 codons with at least four mutations, 31 have ratios of non-silent to silent changes with probabilities less than 0.05 of occurring by chance, and 14 of those have probabilities <0.005. These observations strongly support positive Darwinian selection. We suggest that the small number of variable positions along the successful trunk lineage, together with knowledge of the codons that have shown positive selection, may provide clues that permit an improved prediction of which strains will cause epidemics and therefore should be used for vaccine production.},  Author = {Fitch, W M and Bush, R M and Bender, C A and Cox, N J},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Biological Evolution; Codon; Influenza A virus},  Month = {Jul},  Number = {15},  Pages = {7712-8},  Pmc = {PMC33681},  Pmid = {9223253},  Pst = {ppublish},  Title = {Long term trends in the evolution of H(3) HA1 human influenza type A},  Volume = {94},  Year = {1997}}  @article{Forsberg:2003zr,  Abstract = {Parasites sometimes expand their host range by acquiring a new host species. After a host change event, the selective regime acting on a given parasite gene may change as a result of host-specific adaptive alterations of protein functionality or host-specific immune-mediated selection. We present a codon-based model that attempts to include these effects by allowing the position-specific substitution process to change in conjunction with a host change event. Following maximum-likelihood parameter estimation, we employ an empirical Bayesian procedure to identify candidate sites potentially involved in host-specific adaptation. We discuss the applicability of the model to the more general problem of ascertaining whether the selective regime differs in two groups of related organisms. The utility of the model is illustrated on a data set of nucleoprotein sequences from the influenza A virus obtained from avian and human hosts.},  Author = {Forsberg, Roald and Christiansen, Freddy Bugge},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msg149},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Animals; Codon; Evolution, Molecular; Genetic Variation; Humans; Influenza A virus; Likelihood Functions; Models, Genetic; Phylogeny; Selection, Genetic},  Month = {Aug},  Number = {8},  Pages = {1252-9},  Pmid = {12777510},  Pst = {ppublish},  Title = {A codon-based model of host-specific selection in parasites, with an application to the influenza A virus},  Volume = {20},  Year = {2003},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msg149}}  @article{FRANK:1992ys,  Abstract = {Fisher's Fundamental Theorem of natural selection is one of the most widely cited theories in evolutionary biology. Yet it has been argued that the standard interpretation of the theorem is very different from what Fisher meant to say. What Fisher really meant can be illustrated by looking in a new way at a recent model for the evolution of clutch size. Why Fisher was misunderstood depends, in part, on the contrasting views of evolution promoted by Fisher and Wright.},  Address = {THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB},  Author = {FRANK, SA and SLATKIN, M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Isi = {A1992HF62900007},  Isi-Recid = {78804535},  Isi-Ref-Recids = {62608958 40892372 74072507 28962459 20062755 70601178 44866052 788719 5979615 5346718 10963370 6991375 8969495 75301529 21905356 59804961 64835164 387590 292222},  Journal = {Trends In Ecology \& Evolution},  Month = mar,  Number = {3},  Pages = {92-95},  Publisher = {ELSEVIER SCI LTD},  Times-Cited = {52},  Title = {FISHERS FUNDAMENTAL THEOREM OF NATURAL-SELECTION},  Volume = {7},  Year = {1992},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=A1992HF62900007}}  @article{Fraser:2009fu,  Abstract = {A novel influenza A (H1N1) virus has spread rapidly across the globe. Judging its pandemic potential is difficult with limited data, but nevertheless essential to inform appropriate health responses. By analyzing the outbreak in Mexico, early data on international spread, and viral genetic diversity, we make an early assessment of transmissibility and severity. Our estimates suggest that 23,000 (range 6000 to 32,000) individuals had been infected in Mexico by late April, giving an estimated case fatality ratio (CFR) of 0.4\% (range: 0.3 to 1.8\%) based on confirmed and suspected deaths reported to that time. In a community outbreak in the small community of La Gloria, Veracruz, no deaths were attributed to infection, giving an upper 95\% bound on CFR of 0.6\%. Thus, although substantial uncertainty remains, clinical severity appears less than that seen in the 1918 influenza pandemic but comparable with that seen in the 1957 pandemic. Clinical attack rates in children in La Gloria were twice that in adults (<15 years of age: 61\%; >/=15 years: 29\%). Three different epidemiological analyses gave basic reproduction number (R0) estimates in the range of 1.4 to 1.6, whereas a genetic analysis gave a central estimate of 1.2. This range of values is consistent with 14 to 73 generations of human-to-human transmission having occurred in Mexico to late April. Transmissibility is therefore substantially higher than that of seasonal flu, and comparable with lower estimates of R0 obtained from previous influenza pandemics.},  Author = {Fraser, Christophe and Donnelly, Christl A and Cauchemez, Simon and Hanage, William P and Van Kerkhove, Maria D and Hollingsworth, T D{\'e}irdre and Griffin, Jamie and Baggaley, Rebecca F and Jenkins, Helen E and Lyons, Emily J and Jombart, Thibaut and Hinsley, Wes R and Grassly, Nicholas C and Balloux, Francois and Ghani, Azra C and Ferguson, Neil M and Rambaut, Andrew and Pybus, Oliver G and Lopez-Gatell, Hugo and Alpuche-Aranda, Celia M and Chapela, Ietza Bojorquez and Zavala, Ethel Palacios and Guevara, Dulce Ma Espejo and Checchi, Francesco and Garcia, Erika and Hugonnet, Stephane and Roth, Cathy and {WHO Rapid Pandemic Assessment Collaboration}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2013-08-09 21:44:30 +0000},  Doi = {10.1126/science.1176062},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Disease Outbreaks; Humans; Influenza A Virus, H1N1 Subtype; Influenza, Human; Mexico; Molecular Sequence Data; Travel; World Health},  Month = {Jun},  Number = {5934},  Pages = {1557-61},  Pmid = {19433588},  Pst = {ppublish},  Title = {Pandemic potential of a strain of influenza A ({H1N1}): early findings},  Volume = {324},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1176062}}  @article{Frost:2010fh,  Abstract = {Information on the dynamics of the effective population size over time can be obtained from the analysis of phylogenies, through the application of time-varying coalescent models. This approach has been used to study the dynamics of many different viruses, and has demonstrated a wide variety of patterns, which have been interpreted in the context of changes over time in the 'effective number of infections', a quantity proportional to the number of infected individuals. However, for infectious diseases, the rate of coalescence is driven primarily by new transmissions i.e. the incidence, and only indirectly by the number of infected individuals through sampling effects. Using commonly used epidemiological models, we show that the coalescence rate may indeed reflect the number of infected individuals during the initial phase of exponential growth when time is scaled by infectivity, but in general, a single change in time scale cannot be used to estimate the number of infected individuals. This has important implications when integrating phylogenetic data in the context of other epidemiological data.},  Author = {Frost, Simon D W and Volz, Erik M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1098/rstb.2010.0060},  Journal = {Philos Trans R Soc Lond B Biol Sci},  Journal-Full = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},  Month = {Jun},  Number = {1548},  Pages = {1879-90},  Pmid = {20478883},  Pst = {ppublish},  Title = {Viral phylodynamics and the search for an 'effective number of infections'},  Volume = {365},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rstb.2010.0060}}  @article{Gandon:2009vn,  Abstract = {The mean fitness of a population, often equal to its growth rate, measures its level of adaptation to particular environmental conditions. A better understanding of the evolution of mean fitness could thus provide a natural link between evolution and demography. Yet, after the seminal work of Fisher and its renowned "fundamental theorem of natural selection," the dynamics of mean fitness has attracted little attention, and mostly from theoretical population geneticists. Here we analyze the dynamics of mean fitness in the context of host-parasite interactions. We illustrate the potential relevance of this analysis under different scenarios ranging from a simple situation in which a parasite evolves in a homogeneous host population to a more complex one with host-parasite coevolution. In each case, we contrast the effects of natural selection, recurrent mutations, and the change of the biotic environment, on the dynamics of adaptation. Decoupling these three components helps elucidate the interplay between evolutionary and ecological dynamics. In particular, it offers new perspectives on situations leading to evolutionary suicide. As mean fitness is an easily measurable quantity in microbial systems, this analysis provides new ways to track the dynamics of adaptation in experimental evolution and coevolution studies.},  Author = {Gandon, Sylvain and Day, Troy},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1558-5646.2009.00609.x},  Journal = {Evolution},  Journal-Full = {Evolution; international journal of organic evolution},  Mesh = {Adaptation, Biological; Animals; Epidemiology; Evolution; Host-Parasite Interactions; Models, Biological; Parasites; Selection, Genetic},  Month = {Apr},  Number = {4},  Pages = {826-38},  Pmid = {19154387},  Pst = {ppublish},  Title = {Evolutionary epidemiology and the dynamics of adaptation},  Volume = {63},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1558-5646.2009.00609.x}}  @article{gao:1992hu,  Annote = {{\textless}p{\textgreater}10.1038/358495a0{\textless}/p{\textgreater}},  Author = {Gao, Feng and Yue, Ling and White, Albert T. and Pappas, Peter G. and Barchue, Joseph and Hanson, Aloysius P. and Greene, Bruce M. and Sharp, Paul M. and Shaw, George M. and Hahn, Beatrice H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/358495a0},  Journal = {Nature},  Number = {6386},  Pages = {495--499},  Title = {Human infection by genetically diverse {SIVSM-related} {HIV-2} in West Africa},  Url = {http://dx.doi.org/10.1038/358495a0},  Volume = {358},  Year = {1992},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/358495a0}}  @article{gao:1999or,  Annote = {10.1038/17130},  Author = {Gao, Feng and Bailes, Elizabeth and Robertson, David L. and Chen, Yalu and Rodenburg, Cynthia M. and Michael, Scott F. and Cummins, Larry B. and Arthur, Larry O. and Peeters, Martine and Shaw, George M. and Sharp, Paul M. and Hahn, Beatrice H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/17130},  Issn = {0028-0836},  Journal = {Nature},  Month = feb,  Number = {6718},  Pages = {436--441},  Title = {Origin of {HIV-1} in the chimpanzee Pan troglodytes troglodytes},  Url = {http://dx.doi.org/10.1038/17130},  Volume = {397},  Year = {1999},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/17130}}  @book{Gardiner:2009fk,  Address = {Berlin},  Annote = {LDR 01338cam 2200289 a 4500  001 15442029  005 20091211083223.0  008 080908s2009 gw a b 001 0 eng   906 $a7$bcbc$corignew$d2$eepcn$f20$gy-gencatlg  925 0 $aacquire$b2 shelf copies$xpolicy default  955 $apc17 2008-09-08$axh00 2009-03-17 to USPL/STM$ixh07 2009-05-21 to Dewey$axh13 2009-07-01 copy 2 added$wrd11 2009-08-25$aBarcode 00239708559 returned from bindery 2009-12-11  010 $a 2008936877  020 $a9783540707127 (acid-free paper)  040 $aDLC$cDLC$dDLC  050 00 $aQA274$b.G37 2009  082 00 $a519.2/3$222  100 1 $aGardiner, C. W.$q(Crispin W.),$d1942-  245 10 $aStochastic methods :$ba handbook for the natural and social sciences /$cCrispin W. Gardiner.  250 $a4th ed.  260 $aBerlin :$bSpringer,$cc2009.  300 $axvii, 447 p. :$bill. ;$c25 cm.  490 0 $aSpringer series in synergetics  490 0 $aSpringer complexity  500 $aRev. ed. of: Handbook of stochastic methods for physics, chemistry, and the natural sciences. 3rd ed. c2004.  504 $aIncludes bibliographical references (p. [429]-433) and indexes.  650 0 $aStochastic processes.  700 1 $aGardiner, C. W.$q(Crispin W.),$d1942-$tHandbook of stochastic methods for physics, chemistry, and the natural sciences.  },  Author = {Gardiner, C. W},  Call-Number = {QA274},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Dewey-Call-Number = {519.2/3},  Edition = {4th ed},  Genre = {Stochastic processes},  Isbn = {9783540707127 (acid-free paper)},  Library-Id = {2008936877},  Publisher = {Springer},  Series = {Springer series in synergetics},  Title = {Stochastic methods: a handbook for the natural and social sciences},  Year = {2009}}  @article{Gernhard:2008uq,  Abstract = {We investigate a neutral model for speciation and extinction, the constant rate birth-death process. The process is conditioned to have n extant species today, we look at the tree distribution of the reconstructed trees--i.e. the trees without the extinct species. Whereas the tree shape distribution is well-known and actually the same as under the pure birth process, no analytic results for the speciation times were known. We provide the distribution for the speciation times and calculate the expectations analytically. This characterizes the reconstructed trees completely. We will show how the results can be used to date phylogenies.},  Author = {Gernhard, Tanja},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:53:52 +0000},  Doi = {10.1016/j.jtbi.2008.04.005},  Journal = {J Theor Biol},  Journal-Full = {Journal of theoretical biology},  Mesh = {Algorithms; Animals; Computer Simulation; Genetic Speciation; Genetic Variation; Models, Genetic; Phylogeny},  Month = {8},  Number = {4},  Pages = {769-78},  Pmid = {18538793},  Pst = {ppublish},  Title = {The conditioned reconstructed process},  Volume = {253},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jtbi.2008.04.005}}  @article{gibbs:2001re,  Author = {Gibbs, M. J.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1061662},  Issn = {00368075},  Journal = {Science},  Number = {5536},  Pages = {1842--1845},  Title = {Recombination in the Hemagglutinin Gene of the 1918 {"Spanish} Flu"},  Url = {http://www.sciencemag.org.ezproxy.auckland.ac.nz/cgi/citmgr?gca=sci;293/5536/1842},  Volume = {293},  Year = {2001},  Bdsk-Url-1 = {http://www.sciencemag.org.ezproxy.auckland.ac.nz/cgi/citmgr?gca=sci;293/5536/1842},  Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.1061662}}  @article{gibbs:2006mo,  Author = {Gibbs, M.J. and Gibbs, A.J.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0028-0836},  Journal = {Nature},  Number = {7088},  Pages = {E8},  Publisher = {Nature Publishing Group},  Title = {{Molecular virology: Was the 1918 pandemic caused by a bird flu?}},  Volume = {440},  Year = {2006}}  @article{gibbs:2009wh,  Abstract = {The swine-origin influenza A {(H1N1)} virus that appeared in 2009 and was first found in human beings in Mexico, is a reassortant with at least three parents. Six of the genes are closest in sequence to those of {H1N2} 'triple-reassortant' influenza viruses isolated from pigs in North America around 1999-2000. Its other two genes are from different Eurasian 'avian-like' viruses of pigs; the {NA} gene is closest to {H1N1} viruses isolated in Europe in 1991-1993, and the {MP} gene is closest to {H3N2} viruses isolated in Asia in 1999-2000. The sequences of these genes do not directly reveal the immediate source of the virus as the closest were from isolates collected more than a decade before the human pandemic started. The three parents of the virus may have been assembled in one place by natural means, such as by migrating birds, however the consistent link with pig viruses suggests that human activity was involved. We discuss a published suggestion that unsampled pig herds, the intercontinental live pig trade, together with porous quarantine barriers, generated the reassortant. We contrast that suggestion with the possibility that laboratory errors involving the sharing of virus isolates and cultured cells, or perhaps vaccine production, may have been involved. Gene sequences from isolates that bridge the time and phylogenetic gap between the new virus and its parents will distinguish between these possibilities, and we suggest where they should be sought. It is important that the source of the new virus be found if we wish to avoid future pandemics rather than just trying to minimize the consequences after they have emerged. Influenza virus is a very significant zoonotic pathogen. Public confidence in influenza research, and the agribusinesses that are based on influenza's many hosts, has been eroded by several recent events involving the virus. Measures that might restore confidence include establishing a unified international administrative framework coordinating surveillance, research and commercial work with this virus, and maintaining a registry of all influenza isolates.},  Author = {Gibbs, Adrian and Armstrong, John and Downie, Jean},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Virology Journal},  Number = {1},  Pages = {207},  Title = {From where did the 2009 'swine-origin' influenza A virus {(H1N1)} emerge?},  Url = {http://www.virologyj.com/content/6/1/207},  Volume = {6},  Year = {2009},  Bdsk-Url-1 = {http://www.virologyj.com/content/6/1/207}}  @article{Gibson:1998fk,  Abstract = {Markov chain Monte Carlo methodology is presented for estimating parameters in stochastic compartmental models from incomplete observations of the corresponding Markov process. The methods, which are based on the Metropolis-Hastings algorithm, are developed in the context of epidemic models. Their use is illustrated for the particular case where only susceptible, infective, and removed states are represented using simulated realizations of the process. By comparing estimated likelihoods with theoretical forms, in cases where these can be derived, or with the known model parameters, we show that the methods can be used to provide meaningful estimates of parameters and parameter uncertainty. Potential applications of the techniques are also discussed.},  Address = {GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND},  Author = {Gibson, GJ and Renshaw, E},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Isi = {000072720200002},  Isi-Recid = {104569679},  Isi-Ref-Recids = {82352118 34726962 34705004 83570610 96145029 68104476 90155753 104569680 72811647 101030461 94466653 18098686 78057880 33910483 98421581 54815039 851180 74407156 94466655 78069508 102346235 64261716 86503401 88733239 93959369 99248704 104569681 78543684 98489307},  Journal = {Ima Journal of Mathematics Applied In Medicine and Biology},  Keywords = {stochastic compartment models; parameter estimation; Markov chain Monte Carlo methods; hidden Markov models},  Month = mar,  Number = {1},  Pages = {19--40},  Publisher = {OXFORD UNIV PRESS},  Times-Cited = {45},  Title = {Estimating parameters in stochastic compartmental models using Markov chain methods},  Type = {Proceedings Paper},  Volume = {15},  Year = {1998},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=000072720200002}}  @article{Gifford:2007qo,  Abstract = {With ongoing generation of viral genetic diversity and increasing levels of migration, the global human immunodeficiency virus type 1 (HIV-1) epidemic is becoming increasingly heterogeneous. In this study, we investigate the epidemiological characteristics of 5,675 HIV-1 pol gene sequences sampled from distinct infections in the United Kingdom. These sequences were phylogenetically analyzed in conjunction with 976 complete-genome and 3,201 pol gene reference sequences sampled globally and representing the broad range of HIV-1 genetic diversity, allowing us to estimate the probable geographic origins of the various strains present in the United Kingdom. A statistical analysis of phylogenetic clustering in this data set identified several independent transmission chains within the United Kingdom involving recently introduced strains and indicated that strains more commonly associated with infections acquired heterosexually in East Africa are spreading among men who have sex with men. Coalescent approaches were also used and indicated that the transmission chains that we identify originated in the late 1980s to early 1990s. Similar changes in the epidemiological structuring of HIV epidemics are likely to be taking in place in other industrialized nations with large immigrant populations. The framework implemented here takes advantage of the vast amount of routinely generated HIV-1 sequence data and can provide epidemiological insights not readily obtainable through standard surveillance methods.},  Author = {Gifford, Robert J and de Oliveira, Tulio and Rambaut, Andrew and Pybus, Oliver G and Dunn, David and Vandamme, Anne-Mieke and Kellam, Paul and Pillay, Deenan and {UK Collaborative Group on HIV Drug Resistance}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.00889-07},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Cluster Analysis; Evolution, Molecular; Great Britain; HIV Infections; HIV-1; Humans; Molecular Epidemiology; Phylogeny; Polymorphism, Genetic; Sequence Analysis, DNA; pol Gene Products, Human Immunodeficiency Virus},  Month = {Dec},  Number = {23},  Pages = {13050-6},  Pmc = {PMC2169105},  Pmid = {17898057},  Pst = {ppublish},  Title = {Phylogenetic surveillance of viral genetic diversity and the evolving molecular epidemiology of human immunodeficiency virus type 1},  Volume = {81},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.00889-07}}  @article{Gilbert:2007qa,  Abstract = {HIV-1 group M subtype B was the first HIV discovered and is the predominant variant of AIDS virus in most countries outside of sub-Saharan Africa. However, the circumstances of its origin and emergence remain unresolved. Here we propose a geographic sequence and time line for the origin of subtype B and the emergence of pandemic HIV/AIDS out of Africa. Using HIV-1 gene sequences recovered from archival samples from some of the earliest known Haitian AIDS patients, we find that subtype B likely moved from Africa to Haiti in or around 1966 (1962-1970) and then spread there for some years before successfully dispersing elsewhere. A "pandemic" clade, encompassing the vast majority of non-Haitian subtype B infections in the United States and elsewhere around the world, subsequently emerged after a single migration of the virus out of Haiti in or around 1969 (1966-1972). Haiti appears to have the oldest HIV/AIDS epidemic outside sub-Saharan Africa and the most genetically diverse subtype B epidemic, which might present challenges for HIV-1 vaccine design and testing. The emergence of the pandemic variant of subtype B was an important turning point in the history of AIDS, but its spread was likely driven by ecological rather than evolutionary factors. Our results suggest that HIV-1 circulated cryptically in the United States for approximately 12 years before the recognition of AIDS in 1981.},  Author = {Gilbert, M Thomas P and Rambaut, Andrew and Wlasiuk, Gabriela and Spira, Thomas J and Pitchenik, Arthur E and Worobey, Michael},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1073/pnas.0705329104},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Acquired Immunodeficiency Syndrome; Americas; DNA, Viral; HIV-1; Humans; Molecular Sequence Data; Phylogeny; Time Factors},  Month = {Nov},  Number = {47},  Pages = {18566-70},  Pmc = {PMC2141817},  Pmid = {17978186},  Pst = {ppublish},  Title = {The emergence of HIV/AIDS in the Americas and beyond},  Volume = {104},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0705329104}}  @article{gillespie1976general,  Author = {Gillespie, D.T.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0021-9991},  Journal = {Journal of computational physics},  Number = {4},  Pages = {403--434},  Publisher = {Elsevier},  Title = {A general method for numerically simulating the stochastic time evolution of coupled chemical reactions},  Volume = {22},  Year = {1976}}  @article{gillespie2001approximate,  Author = {Gillespie, D.T.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {The Journal of Chemical Physics},  Pages = {1716},  Title = {Approximate accelerated stochastic simulation of chemically reacting systems},  Volume = {115},  Year = {2001}}  @article{Gordo:2007uq,  Abstract = {The analysis of genetic variation in populations of infectious agents may help us understand their epidemiology and evolution. Here we study a model for assessing the levels and patterns of genetic diversity in populations of infectious agents. The population is structured into many small subpopulations, which correspond to their hosts, that are connected according to a specific type of contact network. We considered different types of networks, including fully connected networks and scale free networks, which have been considered as a model that captures some properties of real contact networks. Infectious agents transmit between hosts, through migration, where they grow and mutate until elimination by the host immune system.},  Author = {Gordo, Isabel and Campos, Paulo R A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1186/1471-2148-7-116},  Journal = {BMC Evol Biol},  Journal-Full = {BMC evolutionary biology},  Mesh = {Animals; Antigenic Variation; Gene Frequency; Genetic Variation; Genetics, Population; Host-Parasite Interactions; Humans; Infection; Models, Genetic; Selection, Genetic},  Pages = {116},  Pmc = {PMC1949404},  Pmid = {17629913},  Pst = {epublish},  Title = {Patterns of genetic variation in populations of infectious agents},  Volume = {7},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2148-7-116}}  @article{Gordo:2009hs,  Abstract = {We introduce a model for assessing the levels and patterns of genetic diversity in pathogen populations, whose epidemiology follows a susceptible-infected-recovered model (SIR). We model the population of pathogens as a metapopulation composed of subpopulations (infected hosts), where pathogens replicate and mutate. Hosts transmit pathogens to uninfected hosts. We show that the level of pathogen variation is well predicted by analytical expressions, such that pathogen neutral molecular variation is bounded by the level of infection and increases with the duration of infection. We then introduce selection in the model and study the invasion probability of a new pathogenic strain whose fitness (R(0)(1+s)) is higher than the fitness of the resident strain (R(0)). We show that this invasion probability is given by the relative increment in R(0) of the new pathogen (s). By analyzing the patterns of genetic diversity in this framework, we identify the molecular signatures during the replacement and compare these with those observed in sequences of influenza A.},  Author = {Gordo, Isabel and Gomes, M Gabriela M and Reis, Daniel G and Campos, Paulo R A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pone.0004876},  Journal = {PLoS One},  Journal-Full = {PloS one},  Mesh = {Evolution; Genetic Variation; Influenza A virus; Models, Biological; Mutation},  Number = {3},  Pages = {e4876},  Pmc = {PMC2653725},  Pmid = {19287490},  Pst = {ppublish},  Title = {Genetic diversity in the SIR model of pathogen evolution},  Volume = {4},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pone.0004876}}  @article{grassly:1997:li,  Author = {Grassly, N. C. and Holmes, E. C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 04:00:26 +0000},  Journal = {Molecular Biology and Evolution},  Number = {3},  Pages = {239--247},  Title = {A likelihood method for the detection of selection and recombination using nucleotide sequences},  Url = {http://mbe.oxfordjournals.org/cgi/content/abstract/14/3/239},  Volume = {14},  Year = {1997},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/14/3/239}}  @article{gray:2009sp,  Author = {Gray, Rebecca R. and Tatem, Andrew J. and Lamers, Susanna and Hou, Wei and Laeyendecker, Oliver and Serwadda, David and Sewankambo, Nelson and Gray, Ronald H. and Wawer, Maria and Quinn, Thomas C. and Goodenow, Maureen M. and Salemi, Marco},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1097/QAD.0b013e32832faf61},  Issn = {0269-9370},  Journal = {{AIDS} {(London,} England)},  Month = sep,  Note = {{PMID:} 19644346 {PMCID:} 2742553},  Number = {14},  Pages = {F9--F17},  Title = {Spatial phylodynamics of {HIV-1} epidemic emergence in east Africa},  Volume = {23},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1097/QAD.0b013e32832faf61}}  @article{Grenfell:2004cr,  Abstract = {A key priority for infectious disease research is to clarify how pathogen genetic variation, modulated by host immunity, transmission bottlenecks, and epidemic dynamics, determines the wide variety of pathogen phylogenies observed at scales that range from individual host to population. We call the melding of immunodynamics, epidemiology, and evolutionary biology required to achieve this synthesis pathogen "phylodynamics." We introduce a phylodynamic framework for the dissection of dynamic forces that determine the diversity of epidemiological and phylogenetic patterns observed in RNA viruses of vertebrates. A central pillar of this model is the Evolutionary Infectivity Profile, which captures the relationship between immune selection and pathogen transmission.},  Author = {Grenfell, Bryan T and Pybus, Oliver G and Gog, Julia R and Wood, James L N and Daly, Janet M and Mumford, Jenny A and Holmes, Edward C},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1090727},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Adaptation, Physiological; Animals; Antigenic Variation; Disease Outbreaks; Evolution; Genetics, Population; Humans; Immunity; Mutation; Phylogeny; Population Dynamics; RNA Virus Infections; RNA Viruses; Selection, Genetic; Time Factors; Vaccination},  Month = {Jan},  Number = {5656},  Pages = {327-32},  Pmid = {14726583},  Pst = {ppublish},  Title = {Unifying the epidemiological and evolutionary dynamics of pathogens},  Volume = {303},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1090727}}  @article{Griffiths1994,  Author = {{Griffiths}, R. C. and Tavar\'{e}, S.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2013-05-14 00:29:59 +0000},  Journal = {Philosophical Transactions of the Royal Society B: Biological Sciences},  Pages = {403--410},  Title = {Sampling theory for neutral alleles in a varying environment},  Volume = {344},  Year = {1994}}  @article{guan:1996em,  Abstract = {Avian influenza A viruses from Asia are recognized as the source of genes that reassorted with human viral genes to generate the Asian/57 {(H2N2)} and Hong Kong/68 {(H3N2)} pandemic strains earlier in this century. Here we report the genetic analysis of avian influenza A {H1N1} viruses recently isolated from pigs in southern China, a host suspected to generate new pandemic strains through gene reassortment events. Each of the eight gene segments was of avian origin. Phylogenetic analysis indicates that these genes form an Asian sublineage of the Eurasian avian lineage, suggesting that these viruses are an independent introduction into pigs in Asia. The presence of avian influenza viruses in pigs in China places them in an optimal position for transmission to humans and may serve as an early warning of the emergence of the next human influenza virus pandemic.},  Author = {Guan, Y and Shortridge, K F and Krauss, S and Li, P H and Kawaoka, Y and Webster, R G},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {{0022-538X}},  Journal = {Journal of Virology},  Keywords = {Animals, Chick Embryo, China, Genotype, Influenza A virus, Influenza A Virus, {H1N1} Subtype, Phylogeny, Swine},  Month = nov,  Note = {{PMID:} 8892928},  Number = {11},  Pages = {8041--8046},  Title = {Emergence of avian {H1N1} influenza viruses in pigs in China},  Url = {http://www.ncbi.nlm.nih.gov/pubmed/8892928},  Volume = {70},  Year = {1996},  Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed/8892928}}  @article{Guindon:2004ys,  Abstract = {The unambiguous footprint of positive Darwinian selection in protein-coding DNA sequences is revealed by an excess of nonsynonymous substitutions over synonymous substitutions compared with the neutral expectation. Methods for analyzing the patterns of nonsynonymous and synonymous substitutions usually rely on stochastic models in which the selection regime may vary across the sequence but remains constant across lineages for any amino acid position. Despite some work that has relaxed the constraint that selection patterns remain constant over time, no model provides a strong statistical framework to deal with switches between selection processes at individual sites during the course of evolution. This paper describes an approach that allows the site-specific selection process to vary along lineages of a phylogenetic tree. The parameters of the switching model of codon substitution are estimated by using maximum likelihood. The analysis of eight HIV-1 env homologous sequence data sets shows that this model provides a significantly better fit to the data than one that does not take into account switches between selection patterns in the phylogeny at individual sites. We also provide strong evidence that the strength and the frequency of occurrence of selection might not be estimated accurately when the site-specific variation of selection regimes is ignored.},  Author = {Guindon, St{\'e}phane and Rodrigo, Allen G and Dyer, Kelly A and Huelsenbeck, John P},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1073/pnas.0402177101},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Amino Acid Substitution; Data Interpretation, Statistical; Gene Products, env; Genetic Variation; HIV-1; Likelihood Functions; Phylogeny; Selection, Genetic; Sequence Analysis, Protein; Sequence Analysis, RNA},  Month = {Aug},  Number = {35},  Pages = {12957-62},  Pmc = {PMC516501},  Pmid = {15326304},  Pst = {ppublish},  Title = {Modeling the site-specific variation of selection patterns along lineages},  Volume = {101},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0402177101}}  @article{hahn:2000ai,  Author = {Hahn, Beatrice H. and Shaw, George M. and De, Kevin M. and Cock and Sharp, Paul M.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.287.5453.607},  Journal = {Science},  Month = jan,  Number = {5453},  Pages = {607--614},  Title = {{AIDS} as a Zoonosis: Scientific and Public Health Implications},  Url = {http://www.sciencemag.org/cgi/content/abstract/287/5453/607},  Volume = {287},  Year = {2000},  Bdsk-Url-1 = {http://www.sciencemag.org/cgi/content/abstract/287/5453/607},  Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.287.5453.607}}  @book{Harvey:1991uq,  Address = {Oxford},  Annote = {LDR 01345cam 2200313 a 4500  001 580387  005 20060719181350.0  008 901012s1991 nyua b 001 0 eng   906 $a7$bcbc$corignew$d1$eocip$f19$gy-gencatlg  955 $apc17 to bt00 10-12-90; bt10 to SCD 10-17-90; ff06 10-22-90; fp28 10-26-90; CIP ver. ta06; to SL 09-09-91  035 $9(DLC) 90021148  010 $a 90021148   020 $a0198546416 (hbk.) :$c$45.00  020 $a0198546408 (pbk.) :$c$18.75  040 $aDLC$cDLC$dDLC  050 00 $aQH366.2$b.H385 1991  082 00 $a575/.0072$220  100 1 $aHarvey, Paul H.,$d1947-  245 14 $aThe comparative method in evolutionary biology /$cPaul H. Harvey, Mark D. Pagel.  260 $aOxford ;$aNew York :$bOxford University Press,$c1991.  300 $aviii, 239 p. :$bill. ;$c24 cm.  440 0 $aOxford series in ecology and evolution  504 $aIncludes bibliographical references (p. [206]-229) and indexes.  650 0 $aEvolution (Biology)  650 0 $aEvolution (Biology)$xResearch$xMethodology.  700 1 $aPagel, Mark D.  856 42 $3Publisher description$uhttp://www.loc.gov/catdir/enhancements/fy0604/90021148-d.html  856 41 $3Table of contents only$uhttp://www.loc.gov/catdir/enhancements/fy0604/90021148-t.html  991 $bc-GenColl$hQH366.2$i.H385 1991$p00015028051$tCopy 1$wBOOKS  },  Author = {Harvey, Paul H. and Pagel, Mark D},  Call-Number = {QH366.2},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-27 15:43:28 +1300},  Dewey-Call-Number = {575/.0072},  Genre = {Evolution (Biology)},  Isbn = {0198546416 (hbk.)},  Library-Id = {90021148},  Publisher = {Oxford University Press},  Title = {The comparative method in evolutionary biology},  Year = {1991},  Bdsk-Url-1 = {http://www.loc.gov/catdir/enhancements/fy0604/90021148-d.html}}  @article{Hedrick:2005uq,  Abstract = {The ratio of the effective population size to adult (or census) population size (Ne/N) is an indicator of the extent of genetic variation expected in a population. It has been suggested that this ratio may be quite low for highly fecund species in which there is a sweepstakes-like chance of reproductive success, known as the Hedgecock effect. Here I show theoretically how the ratio may be quite small when there are only a few successful breeders (Nb) and that in this case, the Ne/N ratio is approximately Nb/N. In other words, high variance in reproductive success within a generation can result in a very low effective population size in an organism with large numbers of adults and consequently a very low Ne/N ratio. This finding appears robust when there is a large proportion of families with exactly two progeny or when there is random variation in progeny numbers among these families.},  Author = {Hedrick, Philip},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Evolution},  Journal-Full = {Evolution; international journal of organic evolution},  Mesh = {Conservation of Natural Resources; Genetic Variation; Genetics, Population; Models, Biological; Population Density; Reproduction},  Month = {Jul},  Number = {7},  Pages = {1596-9},  Pmid = {16153045},  Pst = {ppublish},  Title = {Large variance in reproductive success and the Ne/N ratio},  Volume = {59},  Year = {2005}}  @article{heled:2008ba,  Author = {Heled, J. and Drummond, A. J.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 00:53:30 +0000},  Issn = {1471-2148},  Journal = {BMC Evolutionary Biology},  Number = {1},  Pages = {289},  Publisher = {BioMed Central Ltd},  Title = {{Bayesian inference of population size history from multiple loci}},  Volume = {8},  Year = {2008}}  @article{hirsch:1989af,  Annote = {10.1038/339389a0},  Author = {Hirsch, Vanessa M. and Olmsted, Robert A. and {Murphey-Corb}, Michael and Purcell, Robert H. and Johnson, Philip R.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/339389a0},  Journal = {Nature},  Month = jun,  Number = {6223},  Pages = {389--392},  Title = {An African primate lentivirus {(SIVsmclosely} related to {HIV-2}},  Url = {http://dx.doi.org/10.1038/339389a0},  Volume = {339},  Year = {1989},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/339389a0}}  @article{Ho:1995ve,  Abstract = {Treatment of infected patients with ABT-538, an inhibitor of the protease of human immunodeficiency virus type 1 (HIV-1), causes plasma HIV-1 levels to decrease exponentially (mean half-life, 2.1 +/- 0.4 days) and CD4 lymphocyte counts to rise substantially. Minimum estimates of HIV-1 production and clearance and of CD4 lymphocyte turnover indicate that replication of HIV-1 in vivo is continuous and highly productive, driving the rapid turnover of CD4 lymphocytes.},  Author = {Ho, D D and Neumann, A U and Perelson, A S and Chen, W and Leonard, J M and Markowitz, M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/373123a0},  Journal = {Nature},  Journal-Full = {Nature},  Mesh = {Antiviral Agents; CD4 Lymphocyte Count; CD4-Positive T-Lymphocytes; HIV Infections; HIV Protease Inhibitors; HIV-1; Humans; Kinetics; Ritonavir; Viremia; Virion; Virus Replication},  Month = {Jan},  Number = {6510},  Pages = {123-6},  Pmid = {7816094},  Pst = {ppublish},  Title = {Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection},  Volume = {373},  Year = {1995},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/373123a0}}  @article{holmes:1999ph,  Author = {Holmes, E. C. and Worobey, M and Rambaut, A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 03:57:47 +0000},  Journal = {Molecular Biology and Evolution},  Month = mar,  Number = {3},  Pages = {405--409},  Title = {Phylogenetic evidence for recombination in dengue virus},  Url = {http://mbe.oxfordjournals.org/cgi/content/abstract/16/3/405},  Volume = {16},  Year = {1999},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/16/3/405}}  @article{Holmes:2004qf,  Abstract = {Viruses, especially those with RNA genomes, represent ideal organisms to study the dynamics of microevolutionary change. In particular, their rapid rate of nucleotide substitution means that the epidemiological processes that shape their diversity act on the same time-scale as mutations are fixed in viral populations. Consequently, the branching structure of virus phylogenies provides a unique insight into spatial and temporal dynamics. Herein, I describe the key processes in virus phylogeography. These are generally associated with the relative rates of dispersal among populations and virus-host codivergence (vicariance), and the division between acute (short-term) and persistent (long-term) infections. These processes will be illustrated by important human viruses - HIV, dengue, rabies, polyomavirus JC and human papillomavirus - which display varying spatial and temporal structures and virus-host relationships. Key research questions for the future will also be established.},  Author = {Holmes, Edward C},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Mol Ecol},  Journal-Full = {Molecular ecology},  Mesh = {Dengue Virus; Evolution, Molecular; Geography; HIV; Humans; JC Virus; Mutation; Papillomaviridae; Phylogeny; Population Dynamics; RNA Viruses; Rabies virus},  Month = {Apr},  Number = {4},  Pages = {745-56},  Pmid = {15012753},  Pst = {ppublish},  Title = {The phylogeography of human viruses},  Volume = {13},  Year = {2004}}  @article{holmes:2005wh,  Author = {Holmes, Edward C. and Ghedin, Elodie and Miller, Naomi and Taylor, Jill and Bao, Yiming and George, Kirsten St. and Grenfell, Bryan T. and Salzberg, Steven L. and Fraser, Claire M. and Lipman, David J. and Taubenberger, Jeffery K.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pbio.0030300},  Issn = {1544-9173},  Journal = {{PLoS} Biology},  Number = {9},  Pages = {e300},  Title = {{Whole-Genome} Analysis of Human Influenza A Virus Reveals Multiple Persistent Lineages and Reassortment among Recent {H3N2} Viruses},  Url = {http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371%2Fjournal.pbio.0030300},  Volume = {3},  Year = {2005},  Bdsk-Url-1 = {http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0030300},  Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pbio.0030300}}  @article{holmes:2007wh,  Author = {Holmes, Edward C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1073/pnas.0709179104},  Journal = {Proceedings of the National Academy of Sciences},  Month = nov,  Number = {47},  Pages = {18351 --18352},  Title = {When {HIV} spread afar},  Url = {http://www.pnas.org.ezproxy.auckland.ac.nz/content/104/47/18351.short},  Volume = {104},  Year = {2007},  Bdsk-Url-1 = {http://www.pnas.org.ezproxy.auckland.ac.nz/content/104/47/18351.short},  Bdsk-Url-2 = {http://dx.doi.org/10.1073/pnas.0709179104}}  @article{Holmes:2007zr,  Abstract = {Despite the wealth of data describing the ecological factors that underpin viral emergence, little is known about the evolutionary processes that allow viruses to jump species barriers and establish productive infections in new hosts. Understanding the evolutionary basis to virus emergence is therefore a key research goal and many of the debates in this area can be considered within the rigorous theoretical framework established by evolutionary genetics. In particular, the respective roles played by natural selection and genetic drift in shaping genetic diversity are also of fundamental importance for understanding the nature of viral emergence. Herein, we discuss whether there are evolutionary rules to viral emergence, and especially whether certain types of virus, or those that infect a particular type of host species, are more likely to emerge than others. We stress the complex interplay between rates of viral evolution and the ability to recognize cell receptors from phylogenetically divergent host species. We also emphasize the current lack of convincing data as to whether viral emergence requires adaptation to the new host species during the early stages of infection, or whether it is largely a chance process involving the transmission of a viral strain with the necessary genetic characteristics.},  Author = {Holmes, E C and Drummond, A J},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Curr Top Microbiol Immunol},  Journal-Full = {Current topics in microbiology and immunology},  Mesh = {Adaptation, Physiological; Animals; Communicable Diseases, Emerging; Evolution, Molecular; Humans; Recombination, Genetic; Species Specificity; Virus Diseases; Virus Physiological Phenomena; Viruses; Zoonoses},  Pages = {51-66},  Pmid = {17848060},  Pst = {ppublish},  Title = {The evolutionary genetics of viral emergence},  Volume = {315},  Year = {2007}}  @article{holmes:2008ev,  Author = {Holmes, Edward C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1146/annurev.micro.62.081307.162912},  Issn = {0066-4227},  Journal = {Annual Review of Microbiology},  Number = {1},  Pages = {307--328},  Title = {Evolutionary History and Phylogeography of Human Viruses},  Url = {http://arjournals.annualreviews.org.ezproxy.auckland.ac.nz/doi/abs/10.1146/annurev.micro.62.081307.162912?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dncbi.nlm.nih.gov},  Volume = {62},  Year = {2008},  Bdsk-Url-1 = {http://arjournals.annualreviews.org.ezproxy.auckland.ac.nz/doi/abs/10.1146/annurev.micro.62.081307.162912?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=ncbi.nlm.nih.gov},  Bdsk-Url-2 = {http://dx.doi.org/10.1146/annurev.micro.62.081307.162912}}  @article{holmes:2009di,  Author = {Holmes, Edward C. and Grenfell, Bryan T.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pcbi.1000505},  Journal = {{PLoS} Comput Biol},  Month = oct,  Number = {10},  Pages = {e1000505},  Title = {Discovering the Phylodynamics of {RNA} Viruses},  Url = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1371/journal.pcbi.1000505},  Volume = {5},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1371/journal.pcbi.1000505},  Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pcbi.1000505}}  @article{hon:2008ev,  Abstract = {Bats have been identified as the natural reservoir of severe acute respiratory syndrome {(SARS)-like} and {SARS} coronaviruses {(SLCoV} and {SCoV).} However, previous studies suggested that none of the currently sampled bat {SLCoVs} is the descendant of the direct ancestor of {SCoV,} based on their relatively distant phylogenetic relationship. In this study, evidence of the recombinant origin of the genome of a bat {SLCoV} is demonstrated. We identified a potential recombination breakpoint immediately after the consensus intergenic sequence between open reading frame 1 and the S coding region, suggesting the replication intermediates may participate in the recombination event, as previously speculated for other {CoVs.} Phylogenetic analysis of its parental regions suggests the presence of an uncharacterized {SLCoV} lineage that is phylogenetically closer to {SCoVs} than any of the currently sampled bat {SLCoVs.} Using various Bayesian molecular-clock models, interspecies transfer of this {SLCoV} lineage from bats to the amplifying host (e.g., civets) was estimated to have happened a median of 4.08 years before the {SARS} outbreak. Based on this relatively short window period, we speculate that this uncharacterized {SLCoV} lineage may contain the direct ancestor of {SCoV.} This study sheds light on the possible host bat species of the direct ancestor of {SCoV,} providing valuable information on the scope and focus of surveillance for the origin of {SCoV.}},  Author = {Hon, {Chung-Chau} and Lam, {Tsan-Yuk} and Shi, {Zheng-Li} and Drummond, Alexei J. and Yip, {Chi-Wai} and Zeng, Fanya and Lam, {Pui-Yi} and Leung, Frederick {Chi-Ching}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.01926-07},  Journal = {The Journal of Virology},  Number = {4},  Pages = {1819--1826},  Title = {Evidence of the Recombinant Origin of a Bat Severe Acute Respiratory Syndrome {(SARS)-Like} Coronavirus and Its Implications on the Direct Ancestor of {SARS} Coronavirus},  Url = {http://jvi.asm.org/cgi/content/abstract/82/4/1819},  Volume = {82},  Year = {2008},  Bdsk-Url-1 = {http://jvi.asm.org/cgi/content/abstract/82/4/1819},  Bdsk-Url-2 = {http://dx.doi.org/10.1128/JVI.01926-07}}  @article{Hon:2008vn,  Abstract = {Bats have been identified as the natural reservoir of severe acute respiratory syndrome (SARS)-like and SARS coronaviruses (SLCoV and SCoV). However, previous studies suggested that none of the currently sampled bat SLCoVs is the descendant of the direct ancestor of SCoV, based on their relatively distant phylogenetic relationship. In this study, evidence of the recombinant origin of the genome of a bat SLCoV is demonstrated. We identified a potential recombination breakpoint immediately after the consensus intergenic sequence between open reading frame 1 and the S coding region, suggesting the replication intermediates may participate in the recombination event, as previously speculated for other CoVs. Phylogenetic analysis of its parental regions suggests the presence of an uncharacterized SLCoV lineage that is phylogenetically closer to SCoVs than any of the currently sampled bat SLCoVs. Using various Bayesian molecular-clock models, interspecies transfer of this SLCoV lineage from bats to the amplifying host (e.g., civets) was estimated to have happened a median of 4.08 years before the SARS outbreak. Based on this relatively short window period, we speculate that this uncharacterized SLCoV lineage may contain the direct ancestor of SCoV. This study sheds light on the possible host bat species of the direct ancestor of SCoV, providing valuable information on the scope and focus of surveillance for the origin of SCoV.},  Author = {Hon, Chung-Chau and Lam, Tsan-Yuk and Shi, Zheng-Li and Drummond, Alexei J and Yip, Chi-Wai and Zeng, Fanya and Lam, Pui-Yi and Leung, Frederick Chi-Ching},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.01926-07},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Animals; Base Sequence; Bayes Theorem; Chiroptera; Genome, Viral; Models, Genetic; Molecular Sequence Data; Phylogeny; Recombination, Genetic; SARS Virus},  Month = {Feb},  Number = {4},  Pages = {1819-26},  Pmc = {PMC2258724},  Pmid = {18057240},  Pst = {ppublish},  Title = {Evidence of the recombinant origin of a bat severe acute respiratory syndrome (SARS)-like coronavirus and its implications on the direct ancestor of SARS coronavirus},  Volume = {82},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.01926-07}}  @article{Hozbor:2009fk,  Abstract = {Pertussis continues causing significant morbidity and mortality worldwide. Although its epidemiology has been studied in many developed countries, the current pertussis situation in South America is scarcely known. This review summarizes the most important recent data concerning pertussis in a country of South America, Argentina.},  Author = {Hozbor, D and Mooi, F and Flores, D and Weltman, G and Bottero, D and Fossati, S and Lara, C and Gaillard, M E and Pianciola, L and Zurita, E and Fioriti, A and Archuby, D and Galas, M and Binsztein, N and Regueira, M and Castuma, C and Fingermann, M and Graieb, A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.jinf.2009.07.014},  Journal = {J Infect},  Journal-Full = {The Journal of infection},  Mesh = {Adolescent; Argentina; Bordetella pertussis; Child; Child, Preschool; DNA Fingerprinting; Humans; Immunotherapy, Active; Incidence; Infant; Infant, Newborn; Whooping Cough},  Month = {Oct},  Number = {4},  Pages = {225-31},  Pmid = {19651156},  Pst = {ppublish},  Title = {Pertussis epidemiology in Argentina: trends over 2004-2007},  Volume = {59},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jinf.2009.07.014}}  @incollection{Hudson1990,  Author = {Hudson, R. R.},  Booktitle = {Oxford surveys in evolutionary biology},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 00:44:14 +0000},  Editor = {Futuyma, D and Antonovics, J},  Pages = {1 -- 44},  Publisher = {Oxford University Press, Oxford},  Title = {Gene genealogies and the coalescent process},  Volume = {7},  Year = {1990}}  @article{huelsenbeck:2001ba,  Author = {Huelsenbeck, John P. and Ronquist, Fredrik and Nielsen, Rasmus and Bollback, Jonathan P.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-27 15:44:56 +1300},  Doi = {10.1126/science.1065889},  Journal = {Science},  Month = dec,  Number = {5550},  Pages = {2310--2314},  Title = {Bayesian Inference of Phylogeny and Its Impact on Evolutionary Biology},  Volume = {294},  Year = {2001},  Bdsk-Url-1 = {http://www.sciencemag.org/cgi/content/abstract/294/5550/2310},  Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.1065889}}  @article{huelsenbeck:2004ba,  Abstract = {A common problem in molecular phylogenetics is choosing a model of {DNA} substitution that does a good job of explaining the {DNA} sequence alignment without introducing superfluous parameters. A number of methods have been used to choose among a small set of candidate substitution models, such as the likelihood ratio test, the Akaike Information Criterion {(AIC),} the Bayesian Information Criterion {(BIC),} and Bayes factors. Current implementations of any of these criteria suffer from the limitation that only a small set of models are examined, or that the test does not allow easy comparison of non-nested models. In this article, we expand the pool of candidate substitution models to include all possible time-reversible models. This set includes seven models that have already been described. We show how Bayes factors can be calculated for these models using reversible jump Markov chain Monte Carlo, and apply the method to 16 {DNA} sequence alignments. For each data set, we compare the model with the best Bayes factor to the best models chosen using {AIC} and {BIC.} We find that the best model under any of these criteria is not necessarily the most complicated one; models with an intermediate number of substitution types typically do best. Moreover, almost all of the models that are chosen as best do not constrain a transition rate to be the same as a transversion rate, suggesting that it is the transition/transversion rate bias that plays the largest role in determining which models are selected. Importantly, the reversible jump Markov chain Monte Carlo algorithm described here allows estimation of phylogeny (and other phylogenetic model parameters) to be performed while accounting for uncertainty in the model of {DNA} substitution.},  Author = {Huelsenbeck, John P. and Larget, Bret and Alfaro, Michael E.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msh123},  Journal = {Molecular Biology and Evolution},  Month = jun,  Number = {6},  Pages = {1123--1133},  Title = {Bayesian Phylogenetic Model Selection Using Reversible Jump Markov Chain Monte Carlo},  Url = {http://mbe.oxfordjournals.org/cgi/content/abstract/21/6/1123},  Volume = {21},  Year = {2004},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/21/6/1123},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/msh123}}  @article{Hughes:2009ij,  Abstract = {The heterosexual risk group has become the largest HIV infected group in the United Kingdom during the last 10 years, but little is known of the network structure and dynamics of viral transmission in this group. The overwhelming majority of UK heterosexual infections are of non-B HIV subtypes, indicating viruses originating among immigrants from sub-Saharan Africa. The high rate of HIV evolution, combined with the availability of a very high density sample of viral sequences from routine clinical care has allowed the phylodynamics of the epidemic to be investigated for the first time. Sequences of the viral protease and partial reverse transcriptase coding regions from 11,071 patients infected with HIV of non-B subtypes were studied. Of these, 2774 were closely linked to at least one other sequence by nucleotide distance. Including the closest sequences from the global HIV database identified 296 individuals that were in UK-based groups of 3 or more individuals. There were a total of 8 UK-based clusters of 10 or more, comprising 143/2774 (5\%) individuals, much lower than the figure of 25\% obtained earlier for men who have sex with men (MSM). Sample dates were incorporated into relaxed clock phylogenetic analyses to estimate the dates of internal nodes. From the resulting time-resolved phylogenies, the internode lengths, used as estimates of maximum transmission intervals, had a median of 27 months overall, over twice as long as obtained for MSM (14 months), with only 2\% of transmissions occurring in the first 6 months after infection. This phylodynamic analysis of non-B subtype HIV sequences representing over 40\% of the estimated UK HIV-infected heterosexual population has revealed heterosexual HIV transmission in the UK is clustered, but on average in smaller groups and is transmitted with slower dynamics than among MSM. More effective intervention to restrict the epidemic may therefore be feasible, given effective diagnosis programmes.},  Author = {Hughes, Gareth J and Fearnhill, Esther and Dunn, David and Lycett, Samantha J and Rambaut, Andrew and Leigh Brown, Andrew J and {UK HIV Drug Resistance Collaboration}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.ppat.1000590},  Journal = {PLoS Pathog},  Journal-Full = {PLoS pathogens},  Mesh = {Bayes Theorem; Cluster Analysis; Databases, Genetic; Female; Great Britain; HIV; HIV Infections; HIV Protease; HIV Reverse Transcriptase; Heterosexuality; Humans; Male; Markov Chains; Molecular Epidemiology; Monte Carlo Method; Phylogeny},  Month = {Sep},  Number = {9},  Pages = {e1000590},  Pmc = {PMC2742734},  Pmid = {19779560},  Pst = {ppublish},  Title = {Molecular phylodynamics of the heterosexual HIV epidemic in the United Kingdom},  Volume = {5},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.ppat.1000590}}  @article{huson:1998sp,  Author = {Huson, D.H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {1367-4803},  Journal = {Bioinformatics},  Number = {1},  Pages = {68},  Publisher = {Oxford Univ Press},  Title = {{SplitsTree: analyzing and visualizing evolutionary data.}},  Volume = {14},  Year = {1998}}  @article{jenkins:2002ra,  Annote = {The study of rates of nucleotide substitution in {RNA} viruses is central to our understanding of their evolution. Herein we report a comprehensive analysis of substitution rates in 50 {RNA} viruses using a recently developed maximum likelihood phylogenetic method. This analysis revealed a significant relationship between genetic divergence and isolation time for an extensive array of {RNA} viruses, although more rate variation was usually present among lineages than would be expected under the constraints of a molecular clock. Despite the lack of a molecular clock, the range of statistically significant variation in overall substitution rates was surprisingly narrow for those viruses where a significant relationship between genetic divergence and time was found, as was the case when synonymous sites were considered alone, where the molecular clock was rejected less frequently. An analysis of the ecological and genetic factors that might explain this rate variation revealed some evidence of significantly lower substitution rates in vector-borne viruses, as well as a weak correlation between rate and genome length. Finally, a simulation study revealed that our maximum likelihood estimates of substitution rates are valid, even if the molecular clock is rejected, provided that sufficiently large data sets are analyzed.},  Author = {Jenkins, Gareth M. and Rambaut, Andrew and Pybus, Oliver G. and Holmes, Edward C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0022-2844},  Journal = {Journal of Molecular Evolution},  Keywords = {Biomedical and Life Sciences},  Month = feb,  Number = {2},  Pages = {156--165},  Title = {Rates of Molecular Evolution in {RNA} Viruses: A Quantitative Phylogenetic Analysis},  Url = {http://dx.doi.org/10.1007/s00239-001-0064-3},  Volume = {54},  Year = {2002},  Bdsk-Url-1 = {http://dx.doi.org/10.1007/s00239-001-0064-3}}  @article{Jewell:2009fk,  Abstract = {Mathematical simulation modelling of epidemic processes has recently become a popular tool in guiding policy decisions for potential disease outbreaks. Such models all rely on various parameters in order to specify quantities such as transmission and detection rates. However, the values of these parameters are peculiar to an individual outbreak, and estimating them in advance of an epidemic has been the major difficulty in the predictive credibility of such approaches. The obstruction to classical approaches in estimating model parameters has been that of missing data: (i) an infected individual is only detected after the onset of clinical signs, we never observe the time of infection directly; (ii) if we wish to make inference on an epidemic while it is in progress (in order to predict how it might unfold in the future), we must take into account the fact that there may be individuals who are infected but not yet detected. In this paper we apply a reversible-jump Markov chain Monte Carlo algorithm to a combined spatial and contact network model constructed in a Bayesian context to provide a real-time risk prediction during an epidemic. Using the example of a potential Avian H5N1 epidemic in the UK poultry industry, we demonstrate how such a technique can be used to give real-time predictions of quantities such as the probability of individual poultry holdings becoming infected, the risk that individual holdings pose to the population if they become infected, and the number and whereabouts of infected, but not yet detected, holdings. Since the methodology generalises easily to many epidemic situations, we anticipate its use as a real-time decision-support tool for targetting disease control to critical transmission processes, and for monitoring the efficacy of current control policy.},  Author = {Jewell, C P and Kypraios, T and Christley, R M and Roberts, G O},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.prevetmed.2009.05.019},  Journal = {Prev Vet Med},  Journal-Full = {Preventive veterinary medicine},  Mesh = {Animals; Bayes Theorem; Computer Simulation; Disease Outbreaks; Epidemiologic Methods; Great Britain; Influenza A Virus, H5N1 Subtype; Influenza in Birds; Markov Chains; Models, Biological; Monte Carlo Method; Poultry; Risk Assessment},  Month = {Sep},  Number = {1},  Pages = {19-28},  Pmid = {19535161},  Pst = {ppublish},  Title = {A novel approach to real-time risk prediction for emerging infectious diseases: a case study in Avian Influenza H5N1},  Volume = {91},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.prevetmed.2009.05.019}}  @article{keawcharoen:2004av,  Abstract = {Influenza virus is not known to affect wild felids. We demonstrate that avian influenza A {(H5N1)} virus caused severe pneumonia in tigers and leopards that fed on infected poultry carcasses. This finding extends the host range of influenza virus and has implications for influenza virus epidemiology and wildlife conservation.},  Author = {Keawcharoen, Juthatip and Oraveerakul, Kanisak and Kuiken, Thijs and Fouchier, Ron A M and Amonsin, Alongkorn and Payungporn, Sunchai and Noppornpanth, Suwanna and Wattanodorn, Sumitra and Theambooniers, Apiradee and Tantilertcharoen, Rachod and Pattanarangsan, Rattapan and Arya, Nlin and Ratanakorn, Parntep and Osterhaus, D M E and Poovorawan, Yong},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {1080-6040},  Journal = {Emerging Infectious Diseases},  Keywords = {Animals, Animals, Zoo, Chickens, Food Microbiology, Genetic Variation, Influenza A virus, Influenza A Virus, {H5N1} Subtype, Lung, Meat, Orthomyxoviridae Infections, Panthera, Phylogeny, Tigers},  Month = dec,  Note = {{PMID:} 15663858},  Number = {12},  Pages = {2189--2191},  Title = {Avian influenza {H5N1} in tigers and leopards},  Url = {http://www.ncbi.nlm.nih.gov/pubmed/15663858},  Volume = {10},  Year = {2004},  Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed/15663858}}  @article{keele:2006ch,  Abstract = {Human immunodeficiency virus type 1 {(HIV-1),} the cause of human acquired immunodeficiency syndrome {(AIDS),} is a zoonotic infection of staggering proportions and social impact. Yet uncertainty persists regarding its natural reservoir. The virus most closely related to {HIV-1} is a simian immunodeficiency virus {(SIV)} thus far identified only in captive members of the chimpanzee subspecies Pan troglodytes troglodytes. Here we report the detection of {SIVcpz} antibodies and nucleic acids in fecal samples from wild-living P. t. troglodytes apes in southern Cameroon, where prevalence rates in some communities reached 29 to 35\%. By sequence analysis of endemic {SIVcpz} strains, we could trace the origins of pandemic (group M) and nonpandemic (group N) {HIV-1} to distinct, geographically isolated chimpanzee communities. These findings establish P. t. troglodytes as a natural reservoir of {HIV-1.}},  Author = {Keele, Brandon F. and {Van Heuverswyn}, Fran and Li, Yingying and Bailes, Elizabeth and Takehisa, Jun and Santiago, Mario L. and {Bibollet-Ruche}, Frederic and Chen, Yalu and Wain, Louise V. and Liegeois, Florian and Loul, Severin and Ngole, Eitel Mpoudi and Bienvenue, Yanga and Delaporte, Eric and Brookfield, John F. Y. and Sharp, Paul M. and Shaw, George M. and Peeters, Martine and Hahn, Beatrice H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1126531},  Journal = {Science},  Month = jul,  Number = {5786},  Pages = {523--526},  Title = {Chimpanzee Reservoirs of Pandemic and Nonpandemic {HIV-1}},  Url = {http://www.sciencemag.org/cgi/content/abstract/313/5786/523},  Volume = {313},  Year = {2006},  Bdsk-Url-1 = {http://www.sciencemag.org/cgi/content/abstract/313/5786/523},  Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.1126531}}  @article{Keele:2008mb,  Abstract = {The precise identification of the HIV-1 envelope glycoprotein (Env) responsible for productive clinical infection could be instrumental in elucidating the molecular basis of HIV-1 transmission and in designing effective vaccines. Here, we developed a mathematical model of random viral evolution and, together with phylogenetic tree construction, used it to analyze 3,449 complete env sequences derived by single genome amplification from 102 subjects with acute HIV-1 (clade B) infection. Viral env genes evolving from individual transmitted or founder viruses generally exhibited a Poisson distribution of mutations and star-like phylogeny, which coalesced to an inferred consensus sequence at or near the estimated time of virus transmission. Overall, 78 of 102 subjects had evidence of productive clinical infection by a single virus, and 24 others had evidence of productive clinical infection by a minimum of two to five viruses. Phenotypic analysis of transmitted or early founder Envs revealed a consistent pattern of CCR5 dependence, masking of coreceptor binding regions, and equivalent or modestly enhanced resistance to the fusion inhibitor T1249 and broadly neutralizing antibodies compared with Envs from chronically infected subjects. Low multiplicity infection and limited viral evolution preceding peak viremia suggest a finite window of potential vulnerability of HIV-1 to vaccine-elicited immune responses, although phenotypic properties of transmitted Envs pose a formidable defense.},  Author = {Keele, Brandon F and Giorgi, Elena E and Salazar-Gonzalez, Jesus F and Decker, Julie M and Pham, Kimmy T and Salazar, Maria G and Sun, Chuanxi and Grayson, Truman and Wang, Shuyi and Li, Hui and Wei, Xiping and Jiang, Chunlai and Kirchherr, Jennifer L and Gao, Feng and Anderson, Jeffery A and Ping, Li-Hua and Swanstrom, Ronald and Tomaras, Georgia D and Blattner, William A and Goepfert, Paul A and Kilby, J Michael and Saag, Michael S and Delwart, Eric L and Busch, Michael P and Cohen, Myron S and Montefiori, David C and Haynes, Barton F and Gaschen, Brian and Athreya, Gayathri S and Lee, Ha Y and Wood, Natasha and Seoighe, Cathal and Perelson, Alan S and Bhattacharya, Tanmoy and Korber, Bette T and Hahn, Beatrice H and Shaw, George M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1073/pnas.0802203105},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {AIDS Vaccines; Base Sequence; Disease Transmission, Infectious; Evolution, Molecular; Genetic Variation; HIV Antibodies; HIV Infections; HIV-1; Humans; Models, Biological; Molecular Sequence Data; Mutation; Phylogeny; RNA, Viral; Receptors, CCR5; Sequence Analysis, RNA; env Gene Products, Human Immunodeficiency Virus},  Month = {May},  Number = {21},  Pages = {7552-7},  Pmc = {PMC2387184},  Pmid = {18490657},  Pst = {ppublish},  Title = {Identification and characterization of transmitted and early founder virus envelopes in primary HIV-1 infection},  Volume = {105},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0802203105}}  @article{Keeling:2001kx,  Abstract = {Foot-and-mouth is one of the world's most economically important livestock diseases. We developed an individual farm-based stochastic model of the current UK epidemic. The fine grain of the epidemiological data reveals the infection dynamics at an unusually high spatiotemporal resolution. We show that the spatial distribution, size, and species composition of farms all influence the observed pattern and regional variability of outbreaks. The other key dynamical component is long-tailed stochastic dispersal of infection, combining frequent local movements with occasional long jumps. We assess the history and possible duration of the epidemic, the performance of control strategies, and general implications for disease dynamics in space and time.},  Author = {Keeling, M J and Woolhouse, M E and Shaw, D J and Matthews, L and Chase-Topping, M and Haydon, D T and Cornell, S J and Kappey, J and Wilesmith, J and Grenfell, B T},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1065973},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Animal Husbandry; Animals; Cattle; Cattle Diseases; Disease Outbreaks; Disease Susceptibility; Foot-and-Mouth Disease; Foot-and-Mouth Disease Virus; Great Britain; Models, Biological; Models, Statistical; Sheep; Sheep Diseases; Space-Time Clustering; Stochastic Processes; Vaccination; Viral Vaccines},  Month = {Oct},  Number = {5543},  Pages = {813-7},  Pmid = {11679661},  Pst = {ppublish},  Title = {Dynamics of the 2001 UK foot and mouth epidemic: stochastic dispersal in a heterogeneous landscape},  Volume = {294},  Year = {2001},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1065973}}  @book{Keeling:2008zr,  Address = {Princeton},  Annote = {LDR 01891cam 22004577a 4500  001 14653322  005 20081017103250.0  008 061201s2008 njuab b 001 0 eng   906 $a7$bcbc$ccopycat$d2$encip$f20$gy-gencatlg  925 0 $aacquire$b2 shelf copies$xpolicy default  955 $aja21 2008-08-06 z-processor$ijx85 2008-08-09$ejx85 2008-08-09 to BCCD (two copies)  955 $apc16 2006-12-01  010 $a 2006939548  015 $aGBA761844$2bnb  016 7 $a101321609$2DNLM  016 7 $a013811015$2Uk  020 $a9780691116174 (alk. paper)  020 $a0691116172 (alk. paper)  035 $a(OCoLC)ocn163616681  040 $aNLM$cNLM$dUKM$dBTCTA$dYDXCP$dBAKER$dIXA$dAGL$dCUX$dNDD$dVP@$dDLC  042 $anlmcopyc$alccopycat  050 00 $aRA643$b.K395 2008  060 00 $a2007 L-628  060 10 $aWA 950$bK26m 2008  070 0 $aRA643$b.K43 2008  082 04 $a616.9015118$222  100 1 $aKeeling, Matthew James.  245 10 $aModeling infectious diseases in humans and animals /$cMatt J. Keeling and Pejman Rohani.  260 $aPrinceton :$bPrinceton University Press,$cc2008.  300 $axi, 366 p. :$bill., maps ;$c27 cm.  504 $aIncludes bibliographical references (p. [337]-359) and index.  650 0 $aCommunicable diseases$xMathematical models.  650 0 $aCommunicable diseases in animals$xMathematical models.  650 12 $aEpidemiologic Methods.  650 22 $aCommunicable Disease Control$xmethods.  650 22 $aCommunicable Diseases$xepidemiology.  650 22 $aModels, Theoretical.  700 1 $aRohani, Pejman.  856 41 $3Table of contents only$uhttp://www.loc.gov/catdir/toc/fy0805/2006939548.html  856 42 $3Contributor biographical information$uhttp://www.loc.gov/catdir/enhancements/fy0726/2006939548-b.html  856 42 $3Publisher description$uhttp://www.loc.gov/catdir/enhancements/fy0726/2006939548-d.html  },  Author = {Keeling, Matthew James and Rohani, Pejman},  Call-Number = {RA643},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Dewey-Call-Number = {616.9015118},  Genre = {Communicable diseases},  Isbn = {9780691116174 (alk. paper)},  Library-Id = {2006939548},  Publisher = {Princeton University Press},  Title = {Modeling infectious diseases in humans and animals},  Url = {http://www.loc.gov/catdir/toc/fy0805/2006939548.html},  Year = {2008},  Bdsk-Url-1 = {http://www.loc.gov/catdir/toc/fy0805/2006939548.html}}  @article{Kelly:2003bh,  Abstract = {This article develops a theoretical framework to link dynamical and population genetic models of persistent viral infection. This linkage is useful because, while the dynamical and population genetic theories have developed independently, the biological processes they describe are completely interrelated. Parameters of the dynamical models are important determinants of evolutionary processes such as natural selection and genetic drift. We develop analytical methods, based on coupled differential equations and Markov chain theory, to predict the accumulation of genetic diversity within the viral population as a function of dynamical parameters. These methods are first applied to the standard model of viral dynamics and then generalized to consider the infection of multiple host cell types by the viral population. Each cell type is characterized by specific parameter values. Inclusion of multiple cell types increases the likelihood of persistent infection and can increase the amount of genetic diversity within the viral population. However, the overall rate of gene sequence evolution may actually be reduced.},  Author = {Kelly, John K and Williamson, Scott and Orive, Maria E and Smith, Marilyn S and Holt, Robert D},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1086/375543},  Journal = {Am Nat},  Journal-Full = {The American naturalist},  Mesh = {Evolution; Genetic Variation; Genetics, Population; Markov Chains; Models, Biological; Virus Diseases},  Month = {Jul},  Number = {1},  Pages = {14-28},  Pmid = {12856234},  Pst = {ppublish},  Title = {Linking dynamical and population genetic models of persistent viral infection},  Volume = {162},  Year = {2003},  Bdsk-Url-1 = {http://dx.doi.org/10.1086/375543}}  @article{Keogh:2009fk,  Abstract = {Founder populations in reintroduction programmes can experience a genetic bottleneck simply because of their small size. The influence of reproductive skew brought on by polygynous or polyandrous mating systems in these populations can exacerbate already difficult conservation genetic problems, such as inbreeding depression and loss of adaptive potential. Without an understanding of reproductive skew in a target species, and the effect it can have on genetic diversity retained over generations, long-term conservation goals will be compromised. In this issue of Molecular Ecology, Miller et al. (2009a) test how founder group size and variance in male reproductive success influence the maintenance of genetic diversity following reintroduction on a long-term scale. They evaluated genetic diversity in two wild populations of the iconic New Zealand tuatara (Fig. 1), which differ greatly in population size and genetic diversity, and compared this to genetic diversity in multiple founder populations sourced from both populations. Population viability analysis on the maintenance of genetic diversity over 400 years (10 generations) demonstrated that while the loss of heterozygosity was low when compared with both source populations (1-14\%), the greater the male reproductive skew, the greater the predicted losses of genetic diversity. Importantly however, the loss of genetic diversity was ameliorated after population size exceeded 250 animals, regardless of the level of reproductive skew. This study demonstrates that highly informed conservation decisions could be made when you build on a solid foundation of demographic, natural history and behavioural ecology data. These data, when informed by modern population and genetic analysis, mean that fundamental applied conservation questions (how many animals should make up a founder population?) can be answered accurately and with an eye to the long-term consequences of management decisions.},  Author = {Keogh, J Scott},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1365-294X.2009.04316.x},  Journal = {Mol Ecol},  Journal-Full = {Molecular ecology},  Mesh = {Alleles; Animals; Founder Effect; Genetic Variation; Genetics, Population; Lizards; Loss of Heterozygosity; Male; Microsatellite Repeats; Reproduction},  Month = {Sep},  Number = {18},  Pages = {3761-2},  Pmid = {19761487},  Pst = {ppublish},  Title = {Evolutionary, behavioural and molecular ecology must meet to achieve long-term conservation goals},  Volume = {18},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1365-294X.2009.04316.x}}  @article{kermack1927,  Author = {Kermack, W.O. and McKendrick, A.G.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Proceedings of the Royal Society of London. Series A},  Pages = {700--721},  Title = {A Contribution to the Mathematical Theory of Infections},  Volume = {115},  Year = {1927}}  @article{khiabanian:2009re,  Author = {Khiabanian, Hossein and Trifonov, Vladimir and Rabadan, Raul},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pone.0007366},  Editor = {Stolovitzky, Gustavo},  Issn = {1932-6203},  Journal = {{PLoS} {ONE}},  Number = {10},  Pages = {e7366},  Title = {Reassortment Patterns in Swine Influenza Viruses},  Url = {http://dx.plos.org/10.1371/journal.pone.0007366},  Volume = {4},  Year = {2009},  Bdsk-Url-1 = {http://dx.plos.org/10.1371/journal.pone.0007366},  Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pone.0007366}}  @article{kida:1988or,  Author = {Kida, H},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/0042-6822(88)90405-9},  Issn = {00426822},  Journal = {Virology},  Number = {1},  Pages = {160--166},  Title = {Origin of the hemagglutinin gene of {H3N2} influenza viruses from pigs in China},  Url = {http://linkinghub.elsevier.com/retrieve/pii/0042682288904059},  Volume = {162},  Year = {1988},  Bdsk-Url-1 = {http://linkinghub.elsevier.com/retrieve/pii/0042682288904059},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/0042-6822(88)90405-9}}  @article{Kingman:1982kx,  Author = {Kingman, JFC},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0304-4149},  Journal = {Stochastic processes and their applications},  Number = {3},  Pages = {235--248},  Publisher = {Elsevier},  Title = {{The coalescent}},  Volume = {13},  Year = {1982}}  @article{Kingman:2000kx,  Author = {Kingman, J F},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Australia; Computer Simulation; England; Evolution, Molecular; Fourier Analysis; Genetics, Population; History, 20th Century; Models, Genetic},  Month = {Dec},  Number = {4},  Pages = {1461-3},  Pmc = {PMC1461350},  Pmid = {11102348},  Pst = {ppublish},  Title = {Origins of the coalescent. 1974-1982},  Volume = {156},  Year = {2000}}  @article{kishino:2001:pe,  Abstract = {Rates of molecular evolution vary over time and, hence, among lineages. In contrast, widely used methods for estimating divergence times from molecular sequence data assume constancy of rates. Therefore, methods for estimation of divergence times that incorporate rate variation are attractive. Improvements on a previously proposed Bayesian technique for divergence time estimation are described. New parameterization more effectively captures the phylogenetic structure of rate evolution on a tree. Fossil information and other evidence can now be included in Bayesian analyses in the form of constraints on divergence times. Simulation results demonstrate that the accuracy of divergence time estimation is substantially enhanced when constraints are included.},  Author = {Kishino, Hirohisa and Thorne, Jeffrey L. and Bruno, William J.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Molecular Biology and Evolution},  Number = {3},  Pages = {352--361},  Title = {Performance of a Divergence Time Estimation Method under a Probabilistic Model of Rate Evolution},  Url = {http://mbe.oxfordjournals.org/cgi/content/abstract/18/3/352},  Volume = {18},  Year = {2001},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/18/3/352}}  @article{kishino:2001pe,  Abstract = {Rates of molecular evolution vary over time and, hence, among lineages. In contrast, widely used methods for estimating divergence times from molecular sequence data assume constancy of rates. Therefore, methods for estimation of divergence times that incorporate rate variation are attractive. Improvements on a previously proposed Bayesian technique for divergence time estimation are described. New parameterization more effectively captures the phylogenetic structure of rate evolution on a tree. Fossil information and other evidence can now be included in Bayesian analyses in the form of constraints on divergence times. Simulation results demonstrate that the accuracy of divergence time estimation is substantially enhanced when constraints are included.},  Author = {Kishino, Hirohisa and Thorne, Jeffrey L. and Bruno, William J.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2012-05-18 14:54:25 +1200},  Journal = {Molecular Biology and Evolution},  Number = {3},  Pages = {352--361},  Title = {Performance of a Divergence Time Estimation Method under a Probabilistic Model of Rate Evolution},  Volume = {18},  Year = {2001},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/18/3/352}}  @article{Koelle:2006lo,  Abstract = {Human influenza A (subtype H3N2) is characterized genetically by the limited standing diversity of its hemagglutinin and antigenically by clusters that emerge and replace each other within 2 to 8 years. By introducing an epidemiological model that allows for differences between the genetic and antigenic properties of the virus's hemagglutinin, we show that these patterns can arise from cluster-specific immunity alone. Central to the formulation is a genotype-to-phenotype mapping, based on neutral networks, with antigenic phenotypes, not genotypes, determining the degree of strain cross-immunity. The model parsimoniously explains well-known, as well as previously unremarked, features of interpandemic influenza dynamics and evolution. It captures the observed boom-and-bust pattern of viral evolution, with periods of antigenic stasis during which genetic diversity grows, and with episodic contraction of this diversity during cluster transitions.},  Author = {Koelle, Katia and Cobey, Sarah and Grenfell, Bryan and Pascual, Mercedes},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1132745},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Amino Acid Substitution; Antigenic Variation; Antigens, Viral; Computer Simulation; Cross Reactions; Disease Outbreaks; Disease Susceptibility; Epitopes; Evolution, Molecular; Genotype; Hemagglutinin Glycoproteins, Influenza Virus; Humans; Immunity, Herd; Influenza A Virus, H3N2 Subtype; Influenza, Human; Models, Biological; Models, Statistical; Phenotype; Phylogeny; Point Mutation; Polymorphism, Genetic},  Month = {Dec},  Number = {5807},  Pages = {1898-903},  Pmid = {17185596},  Pst = {ppublish},  Title = {Epochal evolution shapes the phylodynamics of interpandemic influenza A (H3N2) in humans},  Volume = {314},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1132745}}  @article{Koelle:2006nx,  Abstract = {Human influenza A (subtype H3N2) is characterized genetically by the limited standing diversity of its hemagglutinin and antigenically by clusters that emerge and replace each other within 2 to 8 years. By introducing an epidemiological model that allows for differences between the genetic and antigenic properties of the virus's hemagglutinin, we show that these patterns can arise from cluster-specific immunity alone. Central to the formulation is a genotype-to-phenotype mapping, based on neutral networks, with antigenic phenotypes, not genotypes, determining the degree of strain cross-immunity. The model parsimoniously explains well-known, as well as previously unremarked, features of interpandemic influenza dynamics and evolution. It captures the observed boom-and-bust pattern of viral evolution, with periods of antigenic stasis during which genetic diversity grows, and with episodic contraction of this diversity during cluster transitions.},  Author = {Koelle, Katia and Cobey, Sarah and Grenfell, Bryan and Pascual, Mercedes},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1132745},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Amino Acid Substitution; Antigenic Variation; Antigens, Viral; Computer Simulation; Cross Reactions; Disease Outbreaks; Disease Susceptibility; Epitopes; Evolution, Molecular; Genotype; Hemagglutinin Glycoproteins, Influenza Virus; Humans; Immunity, Herd; Influenza A Virus, H3N2 Subtype; Influenza, Human; Models, Biological; Models, Statistical; Phenotype; Phylogeny; Point Mutation; Polymorphism, Genetic},  Month = {Dec},  Number = {5807},  Pages = {1898-903},  Pmid = {17185596},  Pst = {ppublish},  Title = {Epochal evolution shapes the phylodynamics of interpandemic influenza A (H3N2) in humans},  Volume = {314},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1132745}}  @article{Koelle:2010oq,  Abstract = {Understanding the epidemiological and evolutionary dynamics of rapidly evolving pathogens is one of the most challenging problems facing disease ecologists today. To date, many mathematical and individual-based models have provided key insights into the factors that may regulate these dynamics. However, in many of these models, abstractions have been made to the simulated sequences that limit an effective interface with empirical data. This is especially the case for rapidly evolving viruses in which de novo mutations result in antigenically novel variants. With this focus, we present a simple two-tiered 'phylodynamic' model whose purpose is to simulate, along with case data, sequence data that will allow for a more quantitative interface with observed sequence data. The model differs from previous approaches in that it separates the simulation of the epidemiological dynamics (tier 1) from the molecular evolution of the virus's dominant antigenic protein (tier 2). This separation of phenotypic dynamics from genetic dynamics results in a modular model that is computationally simpler and allows sequences to be simulated with specifications such as sequence length, nucleotide composition and molecular constraints. To illustrate its use, we apply the model to influenza A (H3N2) dynamics in humans, influenza B dynamics in humans and influenza A (H3N8) dynamics in equine hosts. In all three of these illustrative examples, we show that the model can simulate sequences that are quantitatively similar in pattern to those empirically observed. Future work should focus on statistical estimation of model parameters for these examples as well as the possibility of applying this model, or variants thereof, to other host-virus systems.},  Author = {Koelle, Katia and Khatri, Priya and Kamradt, Meredith and Kepler, Thomas B},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1098/rsif.2010.0007},  Journal = {J R Soc Interface},  Journal-Full = {Journal of the Royal Society, Interface / the Royal Society},  Month = {Sep},  Number = {50},  Pages = {1257-74},  Pmc = {PMC2894885},  Pmid = {20335193},  Pst = {ppublish},  Title = {A two-tiered model for simulating the ecological and evolutionary dynamics of rapidly evolving viruses, with an application to influenza},  Volume = {7},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rsif.2010.0007}}  @article{Koelle:2010sw,  Abstract = {Understanding the epidemiological and evolutionary dynamics of rapidly evolving pathogens is one of the most challenging problems facing disease ecologists today. To date, many mathematical and individual-based models have provided key insights into the factors that may regulate these dynamics. However, in many of these models, abstractions have been made to the simulated sequences that limit an effective interface with empirical data. This is especially the case for rapidly evolving viruses in which de novo mutations result in antigenically novel variants. With this focus, we present a simple two-tiered 'phylodynamic' model whose purpose is to simulate, along with case data, sequence data that will allow for a more quantitative interface with observed sequence data. The model differs from previous approaches in that it separates the simulation of the epidemiological dynamics (tier 1) from the molecular evolution of the virus's dominant antigenic protein (tier 2). This separation of phenotypic dynamics from genetic dynamics results in a modular model that is computationally simpler and allows sequences to be simulated with specifications such as sequence length, nucleotide composition and molecular constraints. To illustrate its use, we apply the model to influenza A (H3N2) dynamics in humans, influenza B dynamics in humans and influenza A (H3N8) dynamics in equine hosts. In all three of these illustrative examples, we show that the model can simulate sequences that are quantitatively similar in pattern to those empirically observed. Future work should focus on statistical estimation of model parameters for these examples as well as the possibility of applying this model, or variants thereof, to other host-virus systems.},  Author = {Koelle, Katia and Khatri, Priya and Kamradt, Meredith and Kepler, Thomas B},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1098/rsif.2010.0007},  Journal = {J R Soc Interface},  Journal-Full = {Journal of the Royal Society, Interface / the Royal Society},  Month = {Mar},  Pmid = {20335193},  Pst = {aheadofprint},  Title = {A two-tiered model for simulating the ecological and evolutionary dynamics of rapidly evolving viruses, with an application to influenza},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rsif.2010.0007}}  @article{Korber:2000kh,  Abstract = {HIV-1 sequences were analyzed to estimate the timing of the ancestral sequence of the main group of HIV-1, the strains responsible for the AIDS pandemic. Using parallel supercomputers and assuming a constant rate of evolution, we applied maximum-likelihood phylogenetic methods to unprecedented amounts of data for this calculation. We validated our approach by correctly estimating the timing of two historically documented points. Using a comprehensive full-length envelope sequence alignment, we estimated the date of the last common ancestor of the main group of HIV-1 to be 1931 (1915-41). Analysis of a gag gene alignment, subregions of envelope including additional sequences, and a method that relaxed the assumption of a strict molecular clock also supported these results.},  Author = {Korber, B and Muldoon, M and Theiler, J and Gao, F and Gupta, R and Lapedes, A and Hahn, B H and Wolinsky, S and Bhattacharya, T},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Acquired Immunodeficiency Syndrome; Africa; Animals; Confidence Intervals; Consensus Sequence; Disease Outbreaks; Europe; Evolution, Molecular; Genes, env; HIV Envelope Protein gp160; HIV-1; Haiti; Humans; Likelihood Functions; Pan troglodytes; Phylogeny; Simian Acquired Immunodeficiency Syndrome; Simian immunodeficiency virus; Time Factors; United States; Zoonoses},  Month = {Jun},  Number = {5472},  Pages = {1789-96},  Pmid = {10846155},  Pst = {ppublish},  Title = {Timing the ancestor of the HIV-1 pandemic strains},  Volume = {288},  Year = {2000}}  @article{Kouyos:2006xd,  Abstract = {Various studies have attempted to estimate the effective population size of HIV-1 to determine the strength of stochastic effects in within-host evolution. The largely discrepant estimates, the complexity of the concept of the effective population size and the resulting uncertainty about the underlying assumptions make the interpretation of these estimates difficult. Here, we explain the concept and critically assess the current estimates. We discuss the biologically relevant factors that affect the estimate and use of the effective population size. We argue that these factors lead to an underestimation of the effective population size and, thus, to an overestimation of the strength of stochastic effects in HIV-1 evolution.},  Author = {Kouyos, Roger D and Althaus, Christian L and Bonhoeffer, Sebastian},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:54:53 +0000},  Doi = {10.1016/j.tim.2006.10.001},  Journal = {Trends Microbiol},  Journal-Full = {Trends in microbiology},  Mesh = {Evolution, Molecular; HIV-1; Humans; Models, Theoretical; Stochastic Processes},  Month = {12},  Number = {12},  Pages = {507-11},  Pmid = {17049239},  Pst = {ppublish},  Title = {Stochastic or deterministic: what is the effective population size of HIV-1?},  Volume = {14},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tim.2006.10.001}}  @article{Kouyos:2010sh,  Abstract = {BACKGROUND: Sequence data from resistance testing offer unique opportunities to characterize the structure of human immunodeficiency virus (HIV) infection epidemics. METHODS: We analyzed a representative set of HIV type 1 (HIV-1) subtype B pol sequences from 5700 patients enrolled in the Swiss HIV Cohort Study. We pooled these sequences with the same number of sequences from foreign epidemics, inferred a phylogeny, and identified Swiss transmission clusters as clades having a minimal size of 10 and containing >or=80\% Swiss sequences. RESULTS: More than one-half of Swiss patients were included within 60 transmission clusters. Most transmission clusters were significantly dominated by specific transmission routes, which were used to identify the following patient groups: men having sex with men (MSM) (38 transmission clusters; average cluster size, 29 patients) or patients acquiring HIV through heterosexual contact (HETs) and injection drug users (IDUs) (12 transmission clusters; average cluster size, 144 patients). Interestingly, there were no transmission clusters dominated by sequences from HETs only. Although 44\% of all HETs who were infected between 1983 and 1986 clustered with injection drug users, this percentage decreased to 18\% for 2003-2006 (P<.001), indicating a diminishing role of injection drug users in transmission among HETs over time. CONCLUSIONS: Our analysis suggests (1) the absence of a self-sustaining epidemic of HIV-1 subtype B in HETs in Switzerland and (2) a temporally decreasing clustering of HIV infections in HETs and IDUs.},  Author = {Kouyos, Roger D and von Wyl, Viktor and Yerly, Sabine and B{\"o}ni, J{\"u}rg and Taff{\'e}, Patrick and Shah, Cyril and B{\"u}rgisser, Philippe and Klimkait, Thomas and Weber, Rainer and Hirschel, Bernard and Cavassini, Matthias and Furrer, Hansjakob and Battegay, Manuel and Vernazza, Pietro L and Bernasconi, Enos and Rickenbach, Martin and Ledergerber, Bruno and Bonhoeffer, Sebastian and G{\"u}nthard, Huldrych F},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1086/651951},  Journal = {J Infect Dis},  Journal-Full = {The Journal of infectious diseases},  Mesh = {HIV Infections; HIV-1; Heterosexuality; Homosexuality, Male; Humans; Male; Molecular Epidemiology; Phylogeny; Risk Factors; Substance Abuse, Intravenous; Switzerland; Time Factors},  Month = {May},  Number = {10},  Pages = {1488-97},  Pmid = {20384495},  Pst = {ppublish},  Title = {Molecular epidemiology reveals long-term changes in HIV type 1 subtype B transmission in Switzerland},  Volume = {201},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1086/651951}}  @article{Lee:2009jl,  Abstract = {We describe a mathematical model and Monte Carlo (MC) simulation of viral evolution during acute infection. We consider both synchronous and asynchronous processes of viral infection of new target cells. The model enables an assessment of the expected sequence diversity in new HIV-1 infections originating from a single transmitted viral strain, estimation of the most recent common ancestor (MRCA) of the transmitted viral lineage, and estimation of the time to coalesce back to the MRCA. We also calculate the probability of the MRCA being the transmitted virus or an evolved variant. Excluding insertions and deletions, we assume HIV-1 evolves by base substitution without selection pressure during the earliest phase of HIV-1 infection prior to the immune response. Unlike phylogenetic methods that follow a lineage backwards to coalescence, we compare the observed data to a model of the diversification of a viral population forward in time. To illustrate the application of these methods, we provide detailed comparisons of the model and simulations results to 306 envelope sequences obtained from eight newly infected subjects at a single time point. The data from 68 patients were in good agreement with model predictions, and hence compatible with a single-strain infection evolving under no selection pressure. The diversity of the samples from the other two patients was too great to be explained by the model, suggesting multiple HIV-1-strains were transmitted. The model can also be applied to longitudinal patient data to estimate within-host viral evolutionary parameters.},  Author = {Lee, Ha Youn and Giorgi, Elena E and Keele, Brandon F and Gaschen, Brian and Athreya, Gayathri S and Salazar-Gonzalez, Jesus F and Pham, Kimmy T and Goepfert, Paul A and Kilby, J Michael and Saag, Michael S and Delwart, Eric L and Busch, Michael P and Hahn, Beatrice H and Shaw, George M and Korber, Bette T and Bhattacharya, Tanmoy and Perelson, Alan S},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.jtbi.2009.07.038},  Journal = {J Theor Biol},  Journal-Full = {Journal of theoretical biology},  Month = {Nov},  Number = {2},  Pages = {341-60},  Pmc = {PMC2760689},  Pmid = {19660475},  Pst = {ppublish},  Title = {Modeling sequence evolution in acute HIV-1 infection},  Volume = {261},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jtbi.2009.07.038}}  @article{leitner:1996ac,  Abstract = {Phylogenetic analyses are increasingly used in attempts to clarify transmission patterns of human immunodeficiency virus type 1 {(HIV-1),} but there is a continuing discussion about their validity because convergent evolution and transmission of minor {HIV} variants may obscure epidemiological patterns. Here we have studied a unique {HIV-1} transmission cluster consisting of nine infected individuals, for whom the time and direction of each virus transmission was exactly known. Most of the transmissions occurred between 1981 and 1983, and a total of 13 blood samples were obtained approximately 2-12 years later. The p17 gag and env V3 regions of the {HIV-1} genome were directly sequenced from uncultured lymphocytes. A true phylogenetic tree was constructed based on the knowledge about when the transmissions had occurred and when the samples were obtained. This complex, known {HIV-1} transmission history was compared with reconstructed molecular trees, which were calculated from the {DNA} sequences by several commonly used phylogenetic inference methods {[Fitch-Margoliash,} neighbor-joining, minimum-evolution, maximum-likelihood, maximum-parsimony, unweighted pair group method using arithmetic averages {(UPGMA),} and a {Fitch-Margoliash} method assuming a molecular clock {(KITSCH)].} A majority of the reconstructed trees were good estimates of the true phylogeny; 12 of 13 taxa were correctly positioned in the most accurate trees. The choice of gene fragment was found to be more important than the choice of phylogenetic method and substitution model. However, methods that are sensitive to unequal rates of change performed more poorly (such as {UPGMA} and {KITSCH,} which assume a constant molecular clock). The rapidly evolving V3 fragment gave better reconstructions than p17, but a combined data set of both p17 and V3 performed best. The accuracy of the phylogenetic methods justifies their use in {HIV-1} research and argues against convergent evolution and selective transmission of certain virus variants.},  Author = {Leitner, T and Escanilla, D and Franz{\'e}n, C and Uhl{\'e}n, M and Albert, J},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Proceedings of the National Academy of Sciences of the United States of America},  Month = oct,  Number = {20},  Pages = {10864--10869},  Title = {Accurate reconstruction of a known {HIV-1} transmission history by phylogenetic tree analysis},  Url = {http://www.pnas.org/content/93/20/10864.abstract},  Volume = {93},  Year = {1996},  Bdsk-Url-1 = {http://www.pnas.org/content/93/20/10864.abstract}}  @article{lemey:2003tr,  Abstract = {In this study we date the introduction of {HIV-2} into the human population and estimate the epidemic history of {HIV-2} subtype A in {Guinea-Bissau,} the putative geographic origin of {HIV-2.} The evolutionary history of the simian immunodeficiency virussooty {mangabey/HIV-2} lineage was reconstructed by using available database sequences with known sampling dates, and a timescale for this history was calculated by using maximum likelihood methods. The date of the most recent common ancestor of {HIV-2} subtype A strains was estimated to be 1940 $\pm$ 16 and that of B strains was estimated to be 1945 $\pm$ 14. In addition we used coalescent theory to estimate the past population dynamics of {HIV-2} subtype A in a rural population of {Guinea-Bissau.} Parametric and nonparametric estimates of the effective number of infections through time were obtained for an equal sample of gag, pol, and env sequences. Our estimates of the epidemic history of {HIV-2} subtype A in {Guinea-Bissau} show a transition from constant size to rapid exponential growth around 1955--1970. Our analysis provides evidence for a zoonotic transfer of {HIV-2} during the first half of the 20th century and an epidemic initiation in {Guinea-Bissau} that coincides with the independence war (1963--1974), suggesting that war-related changes in sociocultural patterns had a major impact on the {HIV-2} epidemic.},  Author = {Lemey, Philippe and Pybus, Oliver G. and Wang, Bin and Saksena, Nitin K. and Salemi, Marco and Vandamme, {Anne-Mieke}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-27 23:27:17 +1300},  Doi = {10.1073/pnas.0936469100},  Journal = {Proceedings of the National Academy of Sciences of the United States of America},  Month = may,  Number = {11},  Pages = {6588 --6592},  Title = {Tracing the origin and history of the {HIV-2} epidemic},  Volume = {100},  Year = {2003},  Bdsk-Url-1 = {http://www.pnas.org/content/100/11/6588.abstract},  Bdsk-Url-2 = {http://dx.doi.org/10.1073/pnas.0936469100}}  @article{Lemey:2004oq,  Abstract = {HIV-1 group O originated through cross-species transmission of SIV from chimpanzees to humans and has established a relatively low prevalence in Central Africa. Here, we infer the population genetics and epidemic history of HIV-1 group O from viral gene sequence data and evaluate the effect of variable evolutionary rates and recombination on our estimates. First, model selection tools were used to specify suitable evolutionary and coalescent models for HIV group O. Second, divergence times and population genetic parameters were estimated in a Bayesian framework using Markov chain Monte Carlo sampling, under both strict and relaxed molecular clock methods. Our results date the origin of the group O radiation to around 1920 (1890-1940), a time frame similar to that estimated for HIV-1 group M. However, group O infections, which remain almost wholly restricted to Cameroon, show a slower rate of exponential growth during the twentieth century, explaining their lower current prevalence. To explore the effect of recombination, the Bayesian framework is extended to incorporate multiple unlinked loci. Although recombination can bias estimates of the time to the most recent common ancestor, this effect does not appear to be important for HIV-1 group O. In addition, we show that evolutionary rate estimates for different HIV genes accurately reflect differential selective constraints along the HIV genome.},  Author = {Lemey, Philippe and Pybus, Oliver G and Rambaut, Andrew and Drummond, Alexei J and Robertson, David L and Roques, Pierre and Worobey, Michael and Vandamme, Anne-Mieke},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:55:32 +0000},  Doi = {10.1534/genetics.104.026666},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Bayes Theorem; Cameroon; Evolution, Molecular; Genetics, Population; Genome, Viral; HIV-1; Humans; Likelihood Functions; Models, Genetic; Phylogeny; Recombination, Genetic; Species Specificity; Viral Proteins},  Month = {7},  Number = {3},  Pages = {1059-68},  Pmc = {PMC1470933},  Pmid = {15280223},  Pst = {ppublish},  Title = {The molecular population genetics of HIV-1 group O},  Volume = {167},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.104.026666}}  @article{Lemey:2006mi,  Abstract = {The HIV evolutionary processes continuously unfold, leaving a measurable footprint in viral gene sequences. A variety of statistical models and inference techniques have been developed to reconstruct the HIV evolutionary history and to investigate the population genetic processes that shape viral diversity. Remarkably different population genetic forces are at work within and among hosts. Population-level HIV phylogenies are mainly shaped by selectively neutral epidemiologic processes, implying that genealogy-based population genetic inference can be useful to study the HIV epidemic history. Such evolutionary analyses have shed light on the origins of HIV, and on the epidemic spread of viral variants in different geographic locations and in different populations. The HIV genealogies reconstructed from within-host sequences indicate the action of selection pressure. In addition, recombination has a significant impact on HIV genetic diversity. Accurately quantifying both the adaptation rate and the population recombination rate of HIV will contribute to a better understanding of immune escape and drug resistance. Characterizing the impact of HIV transmission on viral genetic diversity will be a key factor in reconciling the different population genetic processes within and among hosts.},  Author = {Lemey, Philippe and Rambaut, Andrew and Pybus, Oliver G},  Date = {2006 Jul-Sep},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {AIDS Rev},  Journal-Full = {AIDS reviews},  Mesh = {Adaptation, Biological; Bayes Theorem; Drug Resistance, Viral; Evolution, Molecular; Genetic Variation; HIV; HIV Infections; Humans; Models, Biological; Phylogeny; Population Dynamics; Selection, Genetic},  Number = {3},  Pages = {125-40},  Pmid = {17078483},  Pst = {ppublish},  Title = {HIV evolutionary dynamics within and among hosts},  Volume = {8},  Year = {2006}}  @article{lemey:2007sy,  Author = {Lemey, Philippe and Pond, Sergei L. Kosakovsky and Drummond, Alexei J. and Pybus, Oliver G. and Shapiro, Beth and Barroso, Helena and Taveira, Nuno and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pcbi.0030029},  Issn = {{1553-734X}},  Journal = {{PLoS} Computational Biology},  Number = {2},  Pages = {e29},  Title = {Synonymous Substitution Rates Predict {HIV} Disease Progression as a Result of Underlying Replication Dynamics},  Url = {http://www.ploscompbiol.org.ezproxy.auckland.ac.nz/article/citationList.action?articleURI=info%3Adoi%2F10.1371%2Fjournal.pcbi.0030029},  Volume = {3},  Year = {2007},  Bdsk-Url-1 = {http://www.ploscompbiol.org.ezproxy.auckland.ac.nz/article/citationList.action?articleURI=info:doi/10.1371/journal.pcbi.0030029},  Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pcbi.0030029}}  @article{Lemey:2007ve,  Abstract = {Upon HIV transmission, some patients develop AIDS in only a few months, while others remain disease free for 20 or more years. This variation in the rate of disease progression is poorly understood and has been attributed to host genetics, host immune responses, co-infection, viral genetics, and adaptation. Here, we develop a new "relaxed-clock" phylogenetic method to estimate absolute rates of synonymous and nonsynonymous substitution through time. We identify an unexpected association between the synonymous substitution rate of HIV and disease progression parameters. Since immune activation is the major determinant of HIV disease progression, we propose that this process can also determine viral generation times, by creating favourable conditions for HIV replication. These conclusions may apply more generally to HIV evolution, since we also observed an overall low synonymous substitution rate for HIV-2, which is known to be less pathogenic than HIV-1 and capable of tempering the detrimental effects of immune activation. Humoral immune responses, on the other hand, are the major determinant of nonsynonymous rate changes through time in the envelope gene, and our relaxed-clock estimates support a decrease in selective pressure as a consequence of immune system collapse.},  Author = {Lemey, Philippe and Kosakovsky Pond, Sergei L and Drummond, Alexei J and Pybus, Oliver G and Shapiro, Beth and Barroso, Helena and Taveira, Nuno and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pcbi.0030029},  Journal = {PLoS Comput Biol},  Journal-Full = {PLoS computational biology},  Mesh = {Amino Acid Sequence; Amino Acid Substitution; Codon; Computer Simulation; DNA Mutational Analysis; Disease Progression; Evolution, Molecular; Genetic Predisposition to Disease; Genetic Variation; HIV Infections; Humans; Models, Genetic; Molecular Sequence Data; Viral Envelope Proteins; Virus Activation; Virus Replication},  Month = {Feb},  Number = {2},  Pages = {e29},  Pmc = {PMC1797821},  Pmid = {17305421},  Pst = {ppublish},  Title = {Synonymous substitution rates predict HIV disease progression as a result of underlying replication dynamics},  Volume = {3},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.0030029}}  @article{lemey:2009re,  Abstract = {Here, we present an analysis of the {H1N1pdm} genetic data sampled over the initial stages in the epidemic. To infer phylodynamic spread in time and space we employ a recently developed Bayesian statistical inference framework {(Lemey} et al., in press). We model spatial diffusion as a continuous-time Markov chain process along time-measured genealogies. In this analysis, we consider 40 locations for which sequence data were available on {06-Aug-2009.} The sampling time interval of the 242 sequences spans from {30-Mar-2009} to {12-Jul-2009.} The Bayesian inference typically results in a posterior distribution of phylogenetic trees, each having an estimate of the epidemic locations at the ancestral nodes in the tree. We summarize these trees using the most representative clustering pattern and annotate these clusters with the most probable location states. We can visualize this information as tree that grows over time, seeding locations each time an ancestral node is inferred to exist at a different location. A Bayes factor test provides statistical support for epidemiological linkage throughout the evolutionary history. We demonstrate how our full probabilistic approach efficiently tracks an epidemic based on viral genetic data as it unfolds across the globe.},  Author = {Lemey, Philippe and Suchard, Marc A. and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 02:09:00 +0000},  Journal = {{PLoS} Currents. Influenza},  Note = {{PMID:} 20029613},  Pages = {RRN1031},  Title = {Reconstructing the initial global spread of a human influenza pandemic: a Bayesian spatial-temporal model for the global spread of {H1N1pdm}},  Year = {2009},  Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed/20029613}}  @article{Lemey:2009uq,  Abstract = {As a key factor in endemic and epidemic dynamics, the geographical distribution of viruses has been frequently interpreted in the light of their genetic histories. Unfortunately, inference of historical dispersal or migration patterns of viruses has mainly been restricted to model-free heuristic approaches that provide little insight into the temporal setting of the spatial dynamics. The introduction of probabilistic models of evolution, however, offers unique opportunities to engage in this statistical endeavor. Here we introduce a Bayesian framework for inference, visualization and hypothesis testing of phylogeographic history. By implementing character mapping in a Bayesian software that samples time-scaled phylogenies, we enable the reconstruction of timed viral dispersal patterns while accommodating phylogenetic uncertainty. Standard Markov model inference is extended with a stochastic search variable selection procedure that identifies the parsimonious descriptions of the diffusion process. In addition, we propose priors that can incorporate geographical sampling distributions or characterize alternative hypotheses about the spatial dynamics. To visualize the spatial and temporal information, we summarize inferences using virtual globe software. We describe how Bayesian phylogeography compares with previous parsimony analysis in the investigation of the influenza A H5N1 origin and H5N1 epidemiological linkage among sampling localities. Analysis of rabies in West African dog populations reveals how virus diffusion may enable endemic maintenance through continuous epidemic cycles. From these analyses, we conclude that our phylogeographic framework will make an important asset in molecular epidemiology that can be easily generalized to infer biogeogeography from genetic data for many organisms.},  Author = {Lemey, Philippe and Rambaut, Andrew and Drummond, Alexei J and Suchard, Marc A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pcbi.1000520},  Journal = {PLoS Comput Biol},  Journal-Full = {PLoS computational biology},  Mesh = {Animals; Bayes Theorem; Computational Biology; Dogs; Geography; Humans; Influenza A Virus, H5N1 Subtype; Influenza, Human; Markov Chains; Models, Biological; Molecular Epidemiology; Phylogeny; Rabies; Rabies virus; Stochastic Processes},  Month = {Sep},  Number = {9},  Pages = {e1000520},  Pmc = {PMC2740835},  Pmid = {19779555},  Pst = {ppublish},  Title = {Bayesian phylogeography finds its roots},  Volume = {5},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.1000520}}  @article{Lemey:2010hc,  Abstract = {Research aimed at understanding the geographic context of evolutionary histories is burgeoning across biological disciplines. Recent endeavors attempt to interpret contemporaneous genetic variation in the light of increasingly detailed geographical and environmental observations. Such interest has promoted the development of phylogeographic inference techniques that explicitly aim to integrate such heterogeneous data. One promising development involves reconstructing phylogeographic history on a continuous landscape. Here, we present a Bayesian statistical approach to infer continuous phylogeographic diffusion using random walk models while simultaneously reconstructing the evolutionary history in time from molecular sequence data. Moreover, by accommodating branch-specific variation in dispersal rates, we relax the most restrictive assumption of the standard Brownian diffusion process and demonstrate increased statistical efficiency in spatial reconstructions of over-dispersed random walks by analyzing both simulated and real viral genetic data. We further illustrate how drawing inference about summary statistics from a fully-specified stochastic process over both sequence evolution and spatial movement reveals important characteristics of a rabies epidemic. Together with recent advances in discrete phylogeographic inference, the continuous model developments furnish a flexible statistical framework for biogeographical reconstructions that is easily expanded upon to accommodate various landscape genetic features.},  Author = {Lemey, Philippe and Rambaut, Andrew and Welch, John J and Suchard, Marc A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msq067},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Month = {Mar},  Pmid = {20203288},  Pst = {aheadofprint},  Title = {Phylogeography takes a relaxed random walk in continuous space and time},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msq067}}  @article{li:2005ba,  Author = {Li, W. and Shi, Z. and Yu, M. and Ren, W. and Smith, C. and Epstein, J.H. and Wang, H. and Crameri, G. and Hu, Z. and Zhang, H. and others},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Science},  Number = {5748},  Pages = {676},  Publisher = {AAAS},  Title = {{Bats are natural reservoirs of SARS-like coronaviruses}},  Volume = {310},  Year = {2005}}  @article{li:2006an,  Author = {Li, W. and Wong, S.K. and Li, F. and Kuhn, J.H. and Huang, I. and others},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0022-538X},  Journal = {Journal of virology},  Number = {9},  Pages = {4211},  Publisher = {Am Soc Microbiol},  Title = {{Animal origins of the severe acute respiratory syndrome coronavirus: insight from ACE2-S-protein interactions}},  Volume = {80},  Year = {2006}}  @article{Li:2010pi,  Abstract = {We explored the timescale, spatial spread, and risk group population structure of HIV-1 subtype B', the cause of explosive blood-borne HIV-1 epidemics among injecting drug users (IDUs) and former plasma donors (FPDs) in Asia. Sequences from FPDs in China formed a distinct monophyletic cluster within subtype B'. Further analysis revealed that subtype B' was founded by a single lineage of pandemic subtype B around 1985. Subsequently, the FPD cluster appears to have derived from a single subtype B' lineage around 1991, corroborating the hypothesis that FPD outbreaks stemmed from the preceding epidemic among IDUs in Southeast Asia, most likely from the Golden-Triangle region.},  Author = {Li, Yue and Uenishi, Rie and Hase, Saiki and Liao, Huanan and Li, Xiao-Jie and Tsuchiura, Takayo and Tee, Kok Keng and Pybus, Oliver G and Takebe, Yutaka},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.virol.2010.03.048},  Journal = {Virology},  Journal-Full = {Virology},  Month = {Jul},  Number = {2},  Pages = {223-7},  Pmid = {20435329},  Pst = {ppublish},  Title = {Explosive HIV-1 subtype B' epidemics in Asia driven by geographic and risk group founder events},  Volume = {402},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.virol.2010.03.048}}  @article{liang:2007hi,  Abstract = {Phylogenetic modeling is computationally challenging and most phylogeny models fit a single phylogeny to a single set of molecular sequences. Individual phylogenetic analyses are typically performed independently using publicly available software that fits a computationally intensive Bayesian model using Markov chain Monte Carlo {(MCMC)} simulation. We develop a Bayesian hierarchical semiparametric regression model to combine multiple phylogenetic analyses of {HIV-1} nucleotide sequences and estimate parameters of interest within and across analyses. We use a mixture of Dirichlet processes as a prior for the parameters to relax inappropriate parametric assumptions and to ensure the prior distribution for the parameters is continuous. We use several reweighting algorithms for combining completed {MCMC} analyses to shrink parameter estimates while adjusting for data set-specific covariates. This avoids constructing a large complex model involving all the original data, which would be computationally challenging and would require rewriting the existing stand-alone software.},  Author = {Liang, {Li-Jung} and Weiss, Robert E.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1541-0420.2007.00753.x},  Journal = {Biometrics},  Number = {3},  Pages = {733--741},  Title = {A Hierarchical Semiparametric Regression Model for Combining {HIV-1} Phylogenetic Analyses Using Iterative Reweighting Algorithms},  Url = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1111/j.1541-0420.2007.00753.x},  Volume = {63},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1111/j.1541-0420.2007.00753.x},  Bdsk-Url-2 = {http://dx.doi.org/10.1111/j.1541-0420.2007.00753.x}}  @article{liao:2009ph,  Annote = {To estimate the epidemic history of {HIV-1} {CRF01\_AE} in Vietnam and adjacent Guangxi, China, we determined near full-length nucleotide sequences of {CRF01\_AE} from a total of 33 specimens collected in 1997-1998 from different geographic regions and risk populations in Vietnam. Phylogenetic and Bayesian molecular clock analyses were performed to estimate the date of origin of {CRF01\_AE} lineages. Our study reconstructs the timescale of {CRF01\_AE} expansion in Vietnam and neighboring regions and suggests that the series of {CRF01\_AE} epidemics in Vietnam arose by the sequential introduction of founder strains into new locations and risk groups. {CRF01\_AE} appears to have been present among heterosexuals in {South-Vietnam} for more than a decade prior to its epidemic spread in the early 1990s. In the late 1980s, the virus spread to {IDUs} in Southern Vietnam and subsequently in the mid-1990s to {IDUs} further north. Our results indicate the northward dissemination of {CRF01\_AE} during this time.},  Author = {Liao, Huanan and Tee, Kok Keng and Hase, Saiki and Uenishi, Rie and Li, {Xiao-Jie} and Kusagawa, Shigeru and Thang, Pham Hong and Hien, Nguyen Tran and Pybus, Oliver G. and Takebe, Yutaka},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1016/j.virol.2009.05.023},  Issn = {0042-6822},  Journal = {Virology},  Keywords = {Bayesian analysis, China, {CRF01\_AE,} Injection drug user, Most recent common ancestor {(MRCA),} Vietnam},  Month = aug,  Number = {1},  Pages = {51--56},  Title = {Phylodynamic analysis of the dissemination of {HIV-1} {CRF01\_AE} in Vietnam},  Url = {http://www.sciencedirect.com/science/article/B6WXR-4WK3YDN-1/2/dde997a80e73e6e012c459f93974a360},  Volume = {391},  Year = {2009},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6WXR-4WK3YDN-1/2/dde997a80e73e6e012c459f93974a360},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.virol.2009.05.023}}  @article{lindstrom:2004ge,  Annote = {{{\textless}p{\textgreater}Phylogenic} analysis of all gene segments of human {H2N2} viruses isolated from 1957 to 1968 was undertaken to better understand the evolution of this virus subtype. Human {H3N2} viruses isolated from 1968 to 1972 were also examined to investigate genetic events associated with their emergence in humans and to identify the putative {H2N2} ancestral virus. All gene segments of human {H2N2} viruses demonstrated divergent evolution into two distinct clades {(I} and {II)} among late {H2N2} isolates. All gene segments of 1968 {H3N2} viruses that were retained from human {H2N2} viruses were most similar to clade I {H2N2} genes. However, genes of both clades were found among {H3N2} isolates of 1969-1971. Unique phylogenic topologies reflected multiple reassortment events among late {H2N2} or {H3N2} viruses that resulted in a variety of different genome constellations. These results suggest that {H2N2} viruses continued to circulate after 1968 and that establishment of {H3N2} viruses in humans was associated with multiple reassortment events that contributed to their genetic diversity.{\textless}/p{\textgreater}},  Author = {Lindstrom, Stephen E. and Cox, Nancy J. and Klimov, Alexander},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1016/j.virol.2004.06.009},  Issn = {0042-6822},  Journal = {Virology},  Keywords = {Evolution, Genome constellation, {H2N2,} {H3N2,} Influenza, Reassortment},  Month = oct,  Number = {1},  Pages = {101--119},  Title = {Genetic analysis of human {H2N2} and early {H3N2} influenza viruses, 1957-1972: evidence for genetic divergence and multiple reassortment events},  Url = {http://www.sciencedirect.com/science/article/B6WXR-4D67B89-1/2/689ed406ac4aa4e34d8875d7dc451935},  Volume = {328},  Year = {2004},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6WXR-4D67B89-1/2/689ed406ac4aa4e34d8875d7dc451935},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.virol.2004.06.009}}  @article{lole:1999:fu,  Abstract = {The development of an effective human immunodeficiency virus type 1 {(HIV-1)} vaccine is likely to depend on knowledge of circulating variants of genes other than the commonly sequenced gag and env genes. In addition, full-genome data are particularly limited for {HIV-1} subtype C, currently the most commonly transmitted subtype in India and worldwide. Likewise, little is known about sequence variation of {HIV-1} in India, the country facing the largest burden of {HIV} worldwide. Therefore, the objective of this study was to clone and characterize the complete genome of {HIV-1} from seroconverters infected with subtype C variants in India. Cocultured {HIV-1} isolates were obtained from six seroincident individuals from Pune, India, and virtually full-length {HIV-1} genomes were amplified, cloned, and sequenced from each. Sequence analysis revealed that five of the six genomes were of subtype C, while one was a mosaic of subtypes A and C, with multiple breakpoints in env, nef, and the 3' long terminal repeat as determined by both maximal [chi]2 analysis and phylogenetic bootstrapping. Sequences were compared for preservation of known cytotoxic T lymphocyte {(CTL)} epitopes. Compared with those of the {HIV-1LAI} sequence, 38\% of well-defined {CTL} epitopes were identical. The proportion of nonconservative substitutions for Env, at 61\%, was higher {(P} {\textless} 0.001) than those for Gag (24\%), Pol (18\%), and Nef (32\%). Therefore, characterized {CTL} epitopes demonstrated substantial differences from subtype B laboratory strains, which were most pronounced in Env. Because these clones were obtained from Indian seroconverters, they are likely to facilitate vaccine-related efforts in India by providing potential antigens for vaccine candidates as well as for assays of vaccine responsiveness.},  Author = {Lole, Kavita S. and Bollinger, Robert C. and Paranjape, Ramesh S. and Gadkari, Deepak and Kulkarni, Smita S. and Novak, Nicole G. and Ingersoll, Roxann and Sheppard, Haynes W. and Ray, Stuart C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {The Journal of Virology},  Number = {1},  Pages = {152--160},  Title = {{Full-Length} Human Immunodeficiency Virus Type 1 Genomes from Subtype {C-Infected} Seroconverters in India, with Evidence of Intersubtype Recombination},  Url = {http://jvi.asm.org/cgi/content/abstract/73/1/152},  Volume = {73},  Year = {1999},  Bdsk-Url-1 = {http://jvi.asm.org/cgi/content/abstract/73/1/152}}  @article{Lopes:2010kx,  Abstract = {Approximate Bayesian computation (ABC) is a recently developed technique for solving problems in Bayesian inference. Although typically less accurate than, for example, the frequently used Markov Chain Monte Carlo (MCMC) methods, they have greater flexibility because they do not require the specification of a likelihood function. For this reason considerable amounts of data can be analysed and more complex models can be used providing, thereby, a potential better fit of the model to the data. Since its first applications in the late 1990s its usage has been steadily increasing. The framework was originally developed to solve problems in population genetics. However, as its efficiency was recognized its popularity increased and, consequently, it started to be used in fields as diverse as phylogenetics, ecology, conservation, molecular evolution and epidemiology. While the ABC algorithm is still being greatly studied and alterations to it are being proposed, the statistical approach has already reached a level of maturity well demonstrated by the number of related computer packages that are being developed. As improved ABC algorithms are proposed, the expansion of the use of this method can only increase. In this paper we are going to depict the context that led to the development of ABC focusing on the field of infectious disease epidemiology. We are then going to describe its current usage in such field and present its most recent developments.},  Author = {Lopes, J S and Beaumont, M A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.meegid.2009.10.010},  Journal = {Infect Genet Evol},  Journal-Full = {Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases},  Month = {Aug},  Number = {6},  Pages = {826-33},  Pmid = {19879976},  Pst = {ppublish},  Title = {ABC: a useful Bayesian tool for the analysis of population data},  Volume = {10},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.meegid.2009.10.010}}  @article{Luciani:2009bd,  Abstract = {Many pathogens associated with chronic infections evolve so rapidly that strains found late in an infection have little in common with the initial strain. This raises questions at different levels of analysis because rapid within-host evolution affects the course of an infection, but it can also affect the possibility for natural selection to act at the between-host level. We present a nested approach that incorporates within-host evolutionary dynamics of a rapidly mutating virus (hepatitis C virus) targeted by a cellular cross-reactive immune response, into an epidemiological perspective. The viral trait we follow is the replication rate of the strain initiating the infection. We find that, even for rapidly evolving viruses, the replication rate of the initial strain has a strong effect on the fitness of an infection. Moreover, infections caused by slowly replicating viruses have the highest infection fitness (i.e., lead to more secondary infections), but strains with higher replication rates tend to dominate within a host in the long-term. We also study the effect of cross-reactive immunity and viral mutation rate on infection life history traits. For instance, because of the stochastic nature of our approach, we can identify factors affecting the outcome of the infection (acute or chronic infections). Finally, we show that anti-viral treatments modify the value of the optimal initial replication rate and that the timing of the treatment administration can have public health consequences due to within-host evolution. Our results support the idea that natural selection can act on the replication rate of rapidly evolving viruses at the between-host level. It also provides a mechanistic description of within-host constraints, such as cross-reactive immunity, and shows how these constraints affect the infection fitness. This model raises questions that can be tested experimentally and underlines the necessity to consider the evolution of quantitative traits to understand the outcome and the fitness of an infection.},  Author = {Luciani, Fabio and Alizon, Samuel},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pcbi.1000565},  Journal = {PLoS Comput Biol},  Journal-Full = {PLoS computational biology},  Mesh = {Algorithms; Antiviral Agents; Computational Biology; Evolution, Molecular; Hepacivirus; Hepatitis C; Host-Pathogen Interactions; Humans; Lymphocyte Activation; Models, Genetic; Mutation; Stochastic Processes; Virus Replication},  Month = {Nov},  Number = {11},  Pages = {e1000565},  Pmc = {PMC2768904},  Pmid = {19911046},  Pst = {ppublish},  Title = {The evolutionary dynamics of a rapidly mutating virus within and between hosts: the case of hepatitis C virus},  Volume = {5},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.1000565}}  @article{maddison:2005ma,  Author = {Maddison, D. R. and Maddison, W. P.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 05:55:59 +0000},  Journal = {Massachusetts: Sinauer Associates, Sunderland},  Title = {{MacClade} 4.08},  Year = {2005}}  @article{Magiorkinis:2009ff,  Abstract = {BACKGROUND: Hepatitis C virus (HCV) is estimated to affect 130-180 million people worldwide. Although its origin is unknown, patterns of viral diversity suggest that HCV genotype 1 probably originated from West Africa. Previous attempts to estimate the spatiotemporal parameters of the virus, both globally and regionally, have suggested that epidemic HCV transmission began in 1900 and grew steadily until the late 1980s. However, epidemiological data suggest that the expansion of HCV may have occurred after the Second World War. The aim of our study was to elucidate the timescale and route of the global spread of HCV. METHODS AND FINDINGS: We show that the rarely sequenced HCV region (E2P7NS2) is more informative for molecular epidemiology studies than the more commonly used NS5B region. We applied phylodynamic methods to a substantial set of new E2P7NS2 and NS5B sequences, together with all available global HCV sequences with information in both of these genomic regions, in order to estimate the timescale and nature of the global expansion of the most prevalent HCV subtypes, 1a and 1b. We showed that transmission of subtypes 1a and 1b "exploded" between 1940 and 1980, with the spread of 1b preceding that of 1a by at least 16 y (95\% confidence interval 15-17). Phylogeographic analysis of all available NS5B sequences suggests that HCV subtypes 1a and 1b disseminated from the developed world to the developing countries. CONCLUSIONS: The evolutionary rate of HCV appears faster than previously suggested. The global spread of HCV coincided with the widespread use of transfused blood and blood products and with the expansion of intravenous drug use but slowed prior to the wide implementation of anti-HCV screening. Differences in the transmission routes associated with subtypes 1a and 1b provide an explanation of the relatively earlier expansion of 1b. Our data show that the most plausible route of the HCV dispersal was from developed countries to the developing world. Please see later in the article for the Editors' Summary.},  Author = {Magiorkinis, Gkikas and Magiorkinis, Emmanouil and Paraskevis, Dimitrios and Ho, Simon Y W and Shapiro, Beth and Pybus, Oliver G and Allain, Jean-Pierre and Hatzakis, Angelos},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pmed.1000198},  Journal = {PLoS Med},  Journal-Full = {PLoS medicine},  Mesh = {Africa; Evolution; Genome, Viral; Genotype; Geography; Hepacivirus; Hepatitis C; Humans; RNA, Viral; World Health},  Month = {Dec},  Number = {12},  Pages = {e1000198},  Pmc = {PMC2795363},  Pmid = {20041120},  Pst = {ppublish},  Title = {The global spread of hepatitis C virus 1a and 1b: a phylodynamic and phylogeographic analysis},  Volume = {6},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pmed.1000198}}  @article{Markov:2009lh,  Abstract = {Understanding the origin and nature of hepatitis C virus (HCV) genetic diversity is critical for improving treatment and vaccine design, and such diversity is the sole source of information about the virus' epidemic history prior to its identification 20 years ago. In this paper, we study the molecular epidemiology of HCV genotype 2 in its region of endemic origin, west and central Africa. Our analysis includes 56 new and highly diverse HCV isolates sampled from infected individuals in Guinea-Bissau. By combining phylogenetic, geographical and epidemiological information, we find a previously unappreciated geographical structure in the diversity of HCV genotype 2, pointing to a history of eastwards spatial spread from the west African coast to Cameroon that took place over several centuries. Molecular clock analysis dates the common ancestor of HCV in Guinea-Bissau to 1470 (1414-1582). The phylogenetic position of isolates from Madagascar and Martinique suggests a role for the historical slave trade in the global dissemination of HCV and of the epidemic subtypes 2a and 2c. Coalescent-based estimates of epidemic growth indicate a rapid 20th-century spread of HCV genotype 2 in Cameroon that is absent in Guinea-Bissau. We discuss this contrast in the context of possible parenteral HCV exposure during public-health campaigns undertaken during the colonial era.},  Author = {Markov, Peter V and Pepin, Jacques and Frost, Eric and Deslandes, Sylvie and Labb{\'e}, Annie-Claude and Pybus, Oliver G},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1099/vir.0.011569-0},  Journal = {J Gen Virol},  Journal-Full = {The Journal of general virology},  Mesh = {Africa; Aged; Evolution, Molecular; Guinea-Bissau; Hepacivirus; Hepatitis C; Humans; Male; Middle Aged; Molecular Epidemiology; Molecular Sequence Data; Phylogeny; Viral Nonstructural Proteins},  Month = {Sep},  Number = {Pt 9},  Pages = {2086-96},  Pmid = {19474244},  Pst = {ppublish},  Title = {Phylogeography and molecular epidemiology of hepatitis C virus genotype 2 in Africa},  Volume = {90},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1099/vir.0.011569-0}}  @article{markov:2009ph,  Author = {Markov, P.V. and Pepin, J. and Frost, E. and Deslandes, S. and Labbe, A.C. and Pybus, O.G.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Journal of General Virology},  Number = {9},  Pages = {2086},  Publisher = {Soc General Microbiol},  Title = {{Phylogeography and molecular epidemiology of hepatitis C virus genotype 2 in Africa}},  Volume = {90},  Year = {2009}}  @article{martin:2005rd,  Abstract = {Summary: {RDP2} is a Windows {95/XP} program that examines nucleotide sequence alignments and attempts to identify recombinant sequences and recombination breakpoints using 10 published recombination detection methods, including {GENECONV,} {BOOTSCAN,} {MAXIMUM} {chi}2, {CHIMAERA} and {SISTER} {SCANNING.} The program enables fast automated analysis of large alignments (up to 300 sequences containing 13 000 sites), and interactive exploration, management and verification of results with different recombination detection and tree drawing methods. Availability: {RDP2} is available free from the {RDP2} website (http://darwin.uvigo.es/rdp/rdp.html) Contact: [email protected] Supplementary information: Detailed descriptions of {RDP2} and the methods it implements are included in the program manual, which can be downloaded from the {RDP2} website.},  Author = {Martin, D. P. and Williamson, C. and Posada, D.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/bioinformatics/bth490},  Journal = {Bioinformatics},  Number = {2},  Pages = {260--262},  Title = {{RDP2:} recombination detection and analysis from sequence alignments},  Url = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/21/2/260},  Volume = {21},  Year = {2005},  Bdsk-Url-1 = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/21/2/260},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/bioinformatics/bth490}}  @article{Mau:1999fk,  Abstract = {We derive a Markov chain to sample from the posterior distribution for a phylogenetic tree given sequence information from the corresponding set of organisms, a stochastic model for these data, and a prior distribution on the space of trees. A transformation of the tree into a canonical cophenetic matrix form suggests a simple and effective proposal distribution for selecting candidate trees close to the current tree in the chain. We illustrate the algorithm with restriction site data on 9 plant species, then extend to DNA sequences from 32 species of fish. The algorithm mixes well in both examples from random starting trees, generating reproducible estimates and credible sets for the path of evolution.},  Author = {Mau, B and Newton, M A and Larget, B},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:55:45 +0000},  Journal = {Biometrics},  Journal-Full = {Biometrics},  Mesh = {Algorithms; Animals; Bayes Theorem; Biometry; DNA; Markov Chains; Monte Carlo Method; Perches; Phylogeny; Plants; Stochastic Processes},  Month = {3},  Number = {1},  Pages = {1-12},  Pmid = {11318142},  Pst = {ppublish},  Title = {Bayesian phylogenetic inference via Markov chain Monte Carlo methods},  Volume = {55},  Year = {1999}}  @article{mauclere:1997se,  Author = {Maucl{\`e}re, P. and Loussert-Ajaka, I. and Damond, F. and Fagot, P. and Souqui{\`e}res, S. and Lobe, M.M. and Keou, F.X.M. and Barr{\'e}-Sinoussi, F. and Saragosti, S. and Brun-V{\'e}zinet, F. and others},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0269-9370},  Journal = {Aids},  Number = {4},  Pages = {445},  Title = {{Serological and virological characterization of HIV-1 group O infection in Cameroon}},  Volume = {11},  Year = {1997}}  @article{Mideo:2008fk,  Abstract = {Nested models (also called embedded models) explicitly link dynamical processes that occur at different scales. Recently there has been considerable interest in linking within- and between-host levels of disease dynamics in the study of pathogen evolution. Here we review the extent to which these nested models have increased our understanding of pathogen evolution. We suggest that, although such models have been useful for determining the nature of tradeoffs between epidemiological parameters and for evaluating the consequences of conflicting selection pressures at different scales, the vast majority of previous results could likely have been obtained without the use of nested models per se. Nevertheless, these models have proven very useful through their highlighting of the importance of within-host disease dynamics on pathogen evolution.},  Author = {Mideo, Nicole and Alizon, Samuel and Day, Troy},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.tree.2008.05.009},  Journal = {Trends Ecol Evol},  Journal-Full = {Trends in ecology \& evolution (Personal edition)},  Mesh = {Communicable Diseases; Evolution; Genetic Predisposition to Disease; Host-Pathogen Interactions; Humans; Models, Biological; Population Dynamics},  Month = {Sep},  Number = {9},  Pages = {511-7},  Pmid = {18657880},  Pst = {ppublish},  Title = {Linking within- and between-host dynamics in the evolutionary epidemiology of infectious diseases},  Volume = {23},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tree.2008.05.009}}  @article{Mideo:2008ud,  Abstract = {Nested models (also called embedded models) explicitly link dynamical processes that occur at different scales. Recently there has been considerable interest in linking within- and between-host levels of disease dynamics in the study of pathogen evolution. Here we review the extent to which these nested models have increased our understanding of pathogen evolution. We suggest that, although such models have been useful for determining the nature of tradeoffs between epidemiological parameters and for evaluating the consequences of conflicting selection pressures at different scales, the vast majority of previous results could likely have been obtained without the use of nested models per se. Nevertheless, these models have proven very useful through their highlighting of the importance of within-host disease dynamics on pathogen evolution.},  Author = {Mideo, Nicole and Alizon, Samuel and Day, Troy},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.tree.2008.05.009},  Journal = {Trends Ecol Evol},  Journal-Full = {Trends in ecology \& evolution (Personal edition)},  Mesh = {Communicable Diseases; Evolution; Genetic Predisposition to Disease; Host-Pathogen Interactions; Humans; Models, Biological; Population Dynamics},  Month = {Sep},  Number = {9},  Pages = {511-7},  Pmid = {18657880},  Pst = {ppublish},  Title = {Linking within- and between-host dynamics in the evolutionary epidemiology of infectious diseases},  Volume = {23},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tree.2008.05.009}}  @article{Miller2010:ep,  Author = {Miller, Joel C. and Davoudi, Bahman and Meza, Rafael and Slim, Anja C. and Pourbohloul, Babak},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {DOI: 10.1016/j.jtbi.2009.08.007},  Issn = {0022-5193},  Journal = {Journal of Theoretical Biology},  Keywords = {Deterministic growth},  Number = {1},  Pages = {107 - 115},  Title = {Epidemics with general generation interval distributions},  Url = {http://www.sciencedirect.com/science/article/B6WMD-4X01PJG-7/2/2efb691da07efb53c6ddc5863c9caadd},  Volume = {262},  Year = {2010},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6WMD-4X01PJG-7/2/2efb691da07efb53c6ddc5863c9caadd},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.jtbi.2009.08.007}}  @article{Minin:2008sm,  Abstract = {Kingman's coalescent process opens the door for estimation of population genetics model parameters from molecular sequences. One paramount parameter of interest is the effective population size. Temporal variation of this quantity characterizes the demographic history of a population. Because researchers are rarely able to choose a priori a deterministic model describing effective population size dynamics for data at hand, nonparametric curve-fitting methods based on multiple change-point (MCP) models have been developed. We propose an alternative to change-point modeling that exploits Gaussian Markov random fields to achieve temporal smoothing of the effective population size in a Bayesian framework. The main advantage of our approach is that, in contrast to MCP models, the explicit temporal smoothing does not require strong prior decisions. To approximate the posterior distribution of the population dynamics, we use efficient, fast mixing Markov chain Monte Carlo algorithms designed for highly structured Gaussian models. In a simulation study, we demonstrate that the proposed temporal smoothing method, named Bayesian skyride, successfully recovers ``true'' population size trajectories in all simulation scenarios and competes well with the MCP approaches without evoking strong prior assumptions. We apply our Bayesian skyride method to 2 real data sets. We analyze sequences of hepatitis C virus contemporaneously sampled in Egypt, reproducing all key known aspects of the viral population dynamics. Next, we estimate the demographic histories of human influenza A hemagglutinin sequences, serially sampled throughout 3 flu seasons.},  Author = {Minin, Vladimir N. and Bloomquist, Erik W. and Suchard, Marc A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msn090},  Eprint = {http://mbe.oxfordjournals.org/content/25/7/1459.full.pdf+html},  Journal = {Molecular Biology and Evolution},  Number = {7},  Pages = {1459-1471},  Title = {{Smooth Skyride through a Rough Skyline: Bayesian Coalescent-Based Inference of Population Dynamics}},  Url = {http://mbe.oxfordjournals.org/content/25/7/1459.abstract},  Volume = {25},  Year = {2008},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/content/25/7/1459.abstract},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/msn090}}  @article{motomura:2003di,  Abstract = {A molecular epidemiological investigation was conducted in two major cities in Myanmar {(Yangon} and Mandalay). The study revealed a unique predominance of {HIV-1} subtype B' {(Thailand} variant of subtype B) among injecting drug users in Yangon, indicating the strong founder effect of this variant. In contrast, multiple lineages of {HIV-1} strains were found in Mandalay, leading to the evolution of various forms of intersubtype recombinants. The results showed independent clusters of {HIV-1} transmission in Myanmar.},  Author = {Motomura, Kazushi and Kusagawa, Shigeru and Lwin, Hla Htut and Thwe, Min and Kato, Kayoko and Oishi, Kazunori and Yamamoto, Naoki and Zaw, Myint and Nagatake, Tsuyoshi and Takebe, Yutaka},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0269-9370},  Journal = {{AIDS}},  Number = {4},  Title = {Different subtype distributions in two cities in Myanmar: evidence for independent clusters of {HIV-1} transmission},  Url = {http://journals.lww.com/aidsonline/Fulltext/2003/03070/Different_subtype_distributions_in_two_cities_in.23.aspx},  Volume = {17},  Year = {2003},  Bdsk-Url-1 = {http://journals.lww.com/aidsonline/Fulltext/2003/03070/Different_subtype_distributions_in_two_cities_in.23.aspx}}  @article{nakajima:1978re,  Author = {Nakajima, K. and Desselberger, U. and Palese, P.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0028-0836},  Journal = {Nature},  Pages = {334--339},  Title = {{Recent human influenza A (H1N1) viruses are closely related genetically to strains isolated in 1950}},  Volume = {274},  Year = {1978}}  @article{neel:2009mo,  Abstract = {Chimpanzees and gorillas are the only non-human primates known to harbor viruses closely related to {HIV-1.} Phylogenetic analyses showed that gorillas acquired {SIVgor} from chimpanzees and viruses from the {SIVcpz/SIVgor} lineage have been transmitted to humans on at least 4 occasions leading to {HIV-1} groups M, N, O and P. To determine the geographic distribution, prevalence and species association of {SIVgor,} we conducted a comprehensive molecular epidemiological survey of wild gorillas in Central Africa. Gorilla faecal samples were collected in the home range of western lowland gorillas (n=2367) and eastern Grauer gorillas (n=183), and tested for {SIVgor} specific antibodies and nucleic acids. {SIVgor} antibody positive samples were identified at two sites in Cameroon, with no evidence of infection at 19 other sites, including three in the range of the eastern gorillas. In Cameroon, based on {DNA} and microsatellite analyses of a subset of samples, we estimated the prevalence of {SIVgor} to be 1.6\% (range 0\% to 4.6\%) which is significantly lower than the prevalence of {SIVcpzPtt} in chimpanzees (5.9\% ; range 0\% to 32\%). All newly identified {SIVgor} strains formed a monophyletic lineage within the {SIVcpz} radiation, closely related to {HIV-1} group O and P, and clustered according to their field site of origin. At one site, there was evidence for intergroup transmission and high intra-group prevalence. These isolated hot-spots of {SIVgor} infected gorilla communities could serve as a source for human infection. The overall low prevalence and sporadic distribution of {SIVgor} could suggest a decline of {SIVgor} in wild populations but it cannot be excluded that {SIVgor} is still more prevalent in other parts of the home range of gorillas.},  Author = {Neel, Cecile and Etienne, Lucie and Li, Yingying and Takehisa, Jun and Rudicell, Rebecca S. and Ndong, Innocent and Moudindo, Joseph and Mebenga, Aime and Esteban, Amandine and {Van Heuverswyn}, Fran and Liegeois, Florian and Kranzusch, Philip J. and Walsh, Peter D. and Sanz, Crickette M. and Morgan, David B. and Ndjango, {Jean-Bosco} N. and Plantier, {Jean-Christophe} and Locatelli, Sabrina and Gonder, Mary K. and Leendertz, Fabian H. and Boesch, Christophe and Todd, Angelique and Delaporte, Eric and Ngole, Eitel Mpoudi and Hahn, Beatrice H. and Peeters, Martine},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.02129-09},  Journal = {The Journal of Virology},  Month = nov,  Pages = {JVI.02129--09},  Title = {Molecular Epidemiology of Simian Immunodeficiency Virus Infection in Wild-living Gorillas},  Url = {http://jvi.asm.org/cgi/content/abstract/JVI.02129-09v1},  Year = {2009},  Bdsk-Url-1 = {http://jvi.asm.org/cgi/content/abstract/JVI.02129-09v1},  Bdsk-Url-2 = {http://dx.doi.org/10.1128/JVI.02129-09}}  @article{nelson:2007ev,  Annote = {10.1038/nrg2053},  Author = {Nelson, Martha I. and Holmes, Edward C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nrg2053},  Issn = {1471-0056},  Journal = {Nat Rev Genet},  Month = mar,  Number = {3},  Pages = {196--205},  Title = {The evolution of epidemic influenza},  Url = {http://dx.doi.org/10.1038/nrg2053},  Volume = {8},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nrg2053}}  @article{nelson:2008mu,  Author = {Nelson, Martha I. and Viboud, C{\'e}cile and Simonsen, Lone and Bennett, Ryan T. and Griesemer, Sara B. and George, Kirsten St. and Taylor, Jill and Spiro, David J. and Sengamalay, Naomi A. and Ghedin, Elodie and Taubenberger, Jeffery K. and Holmes, Edward C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.ppat.1000012},  Editor = {Kawaoka, Yoshihiro},  Issn = {1553-7374},  Journal = {{PLoS} Pathogens},  Number = {2},  Pages = {e1000012},  Title = {Multiple Reassortment Events in the Evolutionary History of {H1N1} Influenza A Virus Since 1918},  Url = {http://dx.plos.org/10.1371/journal.ppat.1000012},  Volume = {4},  Year = {2008},  Bdsk-Url-1 = {http://dx.plos.org/10.1371/journal.ppat.1000012},  Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.ppat.1000012}}  @article{nelson:2009or,  Annote = {Resistance to the adamantane class of antiviral drugs by human {A/H3N2} influenza viruses currently exceeds 90\% in the United States and multiple Asian countries. Adamantane resistance is associated with a single amino acid change {(S31N)} in the M2 protein, which was shown to rapidly disseminate globally in 2005 in association with a genome reassortment event. However, the exact origin of influenza {A/H3N2} viruses carrying the {S31N} mutation has not been characterized, particularly in {South-East} Asia. We therefore conducted a phylogenetic analysis of the {HA,} {NA,} and M1/2 segments of viral isolates collected between 1997 and 2007 from temperate localities in the Northern hemisphere {(New} York State, United States, 492 isolates) and Southern hemisphere {(New} Zealand and Australia, 629 isolates) and a subtropical locality in {South-East} Asia {(Hong} Kong, 281 isolates). We find that although the {S31N} mutation was independently introduced at least 11 times, the vast majority of resistant viruses now circulating globally descend from a single introduction that was first detected in the summer of 2003 in Hong Kong. These resistant viruses were continually detected in Hong Kong throughout 2003-2005, acquired a novel {HA} through reassortment during the first part of 2005, and thereafter spread globally. The emergence and persistence of adamantane resistant viruses in Hong Kong further supports a source-sink model of global influenza virus ecology, in which {South-East} Asia experiences continuous viral activity and repeatedly seeds epidemics in temperate areas.},  Author = {Nelson, Martha I. and Simonsen, Lone and Viboud, C�cile and Miller, Mark A. and Holmes, Edward C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1016/j.virol.2009.03.026},  Issn = {0042-6822},  Journal = {Virology},  Keywords = {Adamantane resistance, Evolution, Global migration, Human influenza A virus, Reassortment},  Month = jun,  Number = {2},  Pages = {270--278},  Title = {The origin and global emergence of adamantane resistant {A/H3N2} influenza viruses},  Url = {http://www.sciencedirect.com/science/article/B6WXR-4W4S30N-1/2/62893b6391b5ae5e5a7385e02f35a1ec},  Volume = {388},  Year = {2009},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6WXR-4W4S30N-1/2/62893b6391b5ae5e5a7385e02f35a1ec},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.virol.2009.03.026}}  @article{nielsen:2009st,  Abstract = {In conventional phylogeographic studies, historical demographic processes are elucidated from the geographical distribution of individuals represented on an inferred gene tree. However, the interpretation of gene trees in this context can be difficult as the same demographic/geographical process can randomly lead to multiple different genealogies. Likewise, the same gene trees can arise under different demographic models. This problem has led to the emergence of many statistical methods for making phylogeographic inferences. A popular phylogeographic approach based on nested clade analysis is challenged by the fact that a certain amount of the interpretation of the data is left to the subjective choices of the user, and it has been argued that the method performs poorly in simulation studies. More rigorous statistical methods based on coalescence theory have been developed. However, these methods may also be challenged by computational problems or poor model choice. In this review, we will describe the development of statistical methods in phylogeographic analysis, and discuss some of the challenges facing these methods.},  Author = {{NIELSEN}, {RASMUS} and {BEAUMONT}, {MARK} A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1365-294X.2008.04059.x},  Journal = {Molecular Ecology},  Number = {6},  Pages = {1034--1047},  Title = {Statistical inferences in phylogeography},  Url = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1111/j.1365-294X.2008.04059.x},  Volume = {18},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1111/j.1365-294X.2008.04059.x},  Bdsk-Url-2 = {http://dx.doi.org/10.1111/j.1365-294X.2008.04059.x}}  @article{Nowak:1990fk,  Abstract = {This paper presents a theory to explain the development of immunodeficiency disease after a long and variable incubation period of infection with HIV-1. Two assumptions are central to the theory: (1) mutation via reverse transcription during viral replication can generate viral strains resistant to neutralization by antibodies specific to earlier mutants in a particular host; (2) the virus can kill the CD4-positive lymphocytes that play a role in mounting an immunological attack directed at the virus. The theory is examined via the development of a mathematical model which reveals that an increasing number of antigenically distinct viral strains may overwhelm the immune system of the host. As the viral diversity increases beyond a certain level the immune system is unable to suppress the population growth of all the strains simultaneously. The intuitive explanation of this pattern of model behaviour lies in the assumption that each virus can kill CD4-positive lymphocytes that are specific to any of the viral strains, but each lymphocyte only directs immunological attack against a single viral strain.(ABSTRACT TRUNCATED AT 250 WORDS)},  Author = {Nowak, M A and May, R M and Anderson, R M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {AIDS},  Journal-Full = {AIDS (London, England)},  Mesh = {Acquired Immunodeficiency Syndrome; Antigenic Variation; Evolution; Genetic Variation; Giant Cells; HIV Antibodies; HIV Antigens; HIV-1; Humans; Models, Biological; Mutation; Time Factors; Vaccination; Virulence},  Month = {Nov},  Number = {11},  Pages = {1095-103},  Pmid = {2282182},  Pst = {ppublish},  Title = {The evolutionary dynamics of HIV-1 quasispecies and the development of immunodeficiency disease},  Volume = {4},  Year = {1990}}  @article{Nowak:1991uq,  Abstract = {Longitudinal studies of patients infected with HIV-1 reveal a long and variable incubation period between infection and the development of AIDS. Data from a small number of infected patients show temporal changes in the number of genetically distinct strains of the virus throughout the incubation period, with a slow but steady rise in diversity during the progression to disease. A mathematical model of the dynamic interaction between viral diversity and the human immune system suggests the existence of an antigen diversity threshold, below which the immune system is able to regulate viral population growth but above which the virus population induces the collapse of the CD4+ lymphocyte population. The model suggests that antigenic diversity is the cause, not a consequence, of immunodeficiency disease. The model is compared with available data, and is used to assess how the timing of the application of chemotherapy or immunotherapy influences the rate of progress to disease.},  Author = {Nowak, M A and Anderson, R M and McLean, A R and Wolfs, T F and Goudsmit, J and May, R M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Acquired Immunodeficiency Syndrome; Base Sequence; CD4-Positive T-Lymphocytes; Computer Simulation; DNA, Viral; HIV Antigens; HIV Core Protein p24; HIV-1; Humans; Immunotherapy; Leukocyte Count; Molecular Sequence Data; Mutation; Oligonucleotides; Time Factors; Vaccination},  Month = {Nov},  Number = {5034},  Pages = {963-9},  Pmid = {1683006},  Pst = {ppublish},  Title = {Antigenic diversity thresholds and the development of AIDS},  Volume = {254},  Year = {1991}}  @article{Nowak:1996kx,  Abstract = {Mathematical models, which are based on a firm understanding of biological interactions, can provide nonintuitive insights into the dynamics of host responses to infectious agents and can suggest new avenues for experimentation. Here, a simple mathematical approach is developed to explore the relation between antiviral immune responses, virus load, and virus diversity. The model results are compared to data on cytotoxic T cell responses and viral diversity in infections with the human T cell leukemia virus (HTLV-1) and the human immunodeficiency virus (HIV-1).},  Author = {Nowak, M A and Bangham, C R},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Antibodies, Viral; Antigenic Variation; Antigens, Viral; Cytokines; Cytotoxicity, Immunologic; Epitopes; Genetic Variation; HIV Infections; HIV-1; HTLV-I Infections; Human T-lymphotropic virus 1; Humans; Models, Biological; Mutation; Population Dynamics; T-Lymphocytes, Cytotoxic; Virus Diseases; Virus Physiological Phenomena; Virus Replication; Viruses},  Month = {Apr},  Number = {5258},  Pages = {74-9},  Pmid = {8600540},  Pst = {ppublish},  Title = {Population dynamics of immune responses to persistent viruses},  Volume = {272},  Year = {1996}}  @book{Nowak:2000vn,  Address = {Oxford},  Annote = {LDR 01377cam 22003014a 4500  001 12018969  005 20060721181728.0  008 000524s2000 enka b 001 0 eng   906 $a7$bcbc$corignew$d1$eocip$f20$gy-gencatlg  925 0 $aacquire$b1 shelf copies$xpolicy default  955 $ato ASCD pc16 05-24-00; jc14 05-26-00; jc02 to technician 05-31-00; jc13 06-01-00; to Dewey 06-01-00; aa05 06-05-00; jc03 CIP ver. and to BCCD 01-31-01  010 $a 00042734   020 $a0198504179 (pbk. : alk. paper)  020 $a0198504187 (hbk. : alk. paper)  040 $aDLC$cDLC$dDLC  042 $apcc  050 00 $aRC114.5$b.N68 2000  082 00 $a616.9/25/015118$221  100 1 $aNowak, M. A.$q(Martin A.)  245 10 $aVirus dynamics :$bmathematical principles of immunology and virology /$cMartin A. Nowak, Robert M. May.  260 $aOxford ;$aNew York :$bOxford University Press,$c2000.  300 $axii, 237 p. :$bill. ;$c24 cm.  504 $aIncludes bibliographical references (p. [209]-232) and index.  650 0 $aVirus diseases$xMathematical models.  650 0 $aImmune response$xMathematical models.  700 1 $aMay, Robert M.$q(Robert McCredie),$d1936-  856 42 $3Publisher description$uhttp://www.loc.gov/catdir/enhancements/fy0610/00042734-d.html  856 41 $3Table of contents only$uhttp://www.loc.gov/catdir/enhancements/fy0610/00042734-t.html  },  Author = {Nowak, M. A and May, Robert M},  Call-Number = {RC114.5},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Dewey-Call-Number = {616.9/25/015118},  Genre = {Virus diseases},  Isbn = {0198504179 (pbk. : alk. paper)},  Library-Id = {00042734},  Publisher = {Oxford University Press},  Title = {Virus dynamics: mathematical principles of immunology and virology},  Url = {http://www.loc.gov/catdir/enhancements/fy0610/00042734-d.html},  Year = {2000},  Bdsk-Url-1 = {http://www.loc.gov/catdir/enhancements/fy0610/00042734-d.html}}  @article{OFallon:2010fk,  Abstract = {Accurate reconstruction of the divergence times among individuals is an essential step toward inferring population parameters from genetic data. However, our ability to reconstruct accurate genealogies is often thwarted by the evolutionary forces we hope to detect, most prominently natural selection. Here, I demonstrate that purifying selection acting at many linked sites can systematically bias current methods of genealogical reconstruction, and I present a new method that corrects for this bias by allowing a class of sites to have a time-dependent rate. The parameters influencing the time dependency can be estimated from the data, allowing for a general method to detect the presence of selected sites and correcting for their distortion of the apparent mutation rate. The method works well under a variety of scenarios, including gamma-distributed selection coefficients as well as entirely neutral evolution. I also compare the performance of the new method to relaxed clock models, and I demonstrate the method on a data set from the mitochondrion of the North Atlantic whale-"louse" Cyamus ovalis.},  Author = {O'Fallon, Brendan D},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msq132},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Amphipoda; Animals; Computer Simulation; DNA, Mitochondrial; Evolution, Molecular; Genetics, Population; Likelihood Functions; Models, Genetic; Mutation; Pedigree; Selection, Genetic},  Month = {Oct},  Number = {10},  Pages = {2406-16},  Pmid = {20513741},  Pst = {ppublish},  Title = {A method to correct for the effects of purifying selection on genealogical inference},  Volume = {27},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msq132}}  @article{OFallon:2010kx,  Abstract = {Most population genetic simulators fall into one of two classes, backward time simulators that quickly generate trees but accommodate only relatively simple selective and demographic regimes, and forward simulators that allow for a broader range of evolutionary scenarios but which cannot produce genealogies. Thus, few tools are available that allow for producing genealogies under arbitrarily complex selective and demographic models.},  Author = {O'Fallon, Brendan},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/bioinformatics/btq355},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Mesh = {Biological Evolution; Computer Simulation; Genetics, Population; Models, Genetic; Software; User-Computer Interface},  Month = {Sep},  Number = {17},  Pages = {2200-1},  Pmid = {20671150},  Pst = {ppublish},  Title = {TreesimJ: a flexible, forward time population genetic simulator},  Volume = {26},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/btq355}}  @article{OFallon:2010uq,  Abstract = {Coalescent theory provides an elegant and powerful method for understanding the shape of gene genealogies and resulting patterns of genetic diversity. However, the coalescent does not naturally accommodate the effects of heritable variation in fitness. Although some methods are available for studying the effects of strong selection (Ns >> 1), few tools beyond forward simulation are available for quantifying the impact of weak selection at many sites. Here, we introduce a continuous-state coalescent capable of accurately describing the distortions to genealogies caused by moderate to weak natural selection affecting many linked sites. We calculate approximately the full distribution of pairwise coalescent times, the lengths of coalescent intervals, and the time to the most recent common ancestor of a sample. Weak selection (Ns approximately 1) is found to substantially decrease the tree depth, primarily through a shortening of the lengths of the basal coalescent intervals. Additionally, we demonstrate that only two parameters, population size and the variance of the distribution describing fitness heritability, are sufficient to describe most changes.},  Author = {O'Fallon, Brendan D and Seger, Jon and Adler, Frederick R},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msq006},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Computational Biology; Computer Simulation; Genes; Inheritance Patterns; Models, Genetic; Phylogeny; Selection, Genetic; Time Factors},  Month = {May},  Number = {5},  Pages = {1162-72},  Pmid = {20097659},  Pst = {ppublish},  Title = {A continuous-state coalescent and the impact of weak selection on the structure of gene genealogies},  Volume = {27},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msq006}}  @article{Oliveira:2006il,  Abstract = {In 1998, outbreaks of human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) infection were reported in children attending Al-Fateh Hospital in Benghazi, Libya. Here we use molecular phylogenetic techniques to analyse new virus sequences from these outbreaks. We find that the HIV-1 and HCV strains were already circulating and prevalent in this hospital and its environs before the arrival in March 1998 of the foreign medical staff (five Bulgarian nurses and a Palestinian doctor) who stand accused of transmitting the HIV strain to the children.},  Author = {de Oliveira, Tulio and Pybus, Oliver G and Rambaut, Andrew and Salemi, Marco and Cassol, Sharon and Ciccozzi, Massimo and Rezza, Giovanni and Gattinara, Guido Castelli and D'Arrigo, Roberta and Amicosante, Massimo and Perrin, Luc and Colizzi, Vittorio and Perno, Carlo Federico and {Benghazi Study Group}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Nature},  Journal-Full = {Nature},  Mesh = {Child; HIV Infections; HIV-1; Hepacivirus; Hepatitis C; Humans; Libya; Nurses; Phylogeny; Physicians; Reproducibility of Results},  Month = {Dec},  Number = {7121},  Pages = {836-7},  Pmid = {17171825},  Pst = {ppublish},  Title = {Molecular epidemiology: HIV-1 and HCV sequences from Libyan outbreak},  Volume = {444},  Year = {2006}}  @article{ONeill:2001kx,  Abstract = {A stochastic epidemic model featuring fixed-length latent periods, gamma-distributed infectious periods and randomly varying heterogeneity among susceptibles is considered. A Markov chain Monte Carlo algorithm is developed for performing Bayesian inference for the parameters governing the infectious-period length and the hyper-parameters governing the heterogeneity of susceptibility. This method of analysis applies to a wider class of diseases than methods proposed previously. An application to smallpox data confirms results about heterogeneity suggested by an earlier analysis that relied on less realistic assumptions.},  Author = {O'Neill, P D and Becker, N G},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/biostatistics/2.1.99},  Journal = {Biostatistics},  Journal-Full = {Biostatistics (Oxford, England)},  Month = {Mar},  Number = {1},  Pages = {99-108},  Pmid = {12933559},  Pst = {ppublish},  Title = {Inference for an epidemic when susceptibility varies},  Volume = {2},  Year = {2001},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/biostatistics/2.1.99}}  @article{opgen:2005in,  Author = {Opgen-Rhein, R. and Fahrmeir, L. and Strimmer, K.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {1471-2148},  Journal = {BMC Evolutionary Biology},  Number = {1},  Pages = {6},  Publisher = {BioMed Central Ltd},  Title = {{Inference of demographic history from genealogical trees using reversible jump Markov chain Monte Carlo}},  Volume = {5},  Year = {2005}}  @article{ou:1993in,  Annote = {To investigate the genetic heterogeneity and epidemiological distribution of human immunodeficiency virus type 1 {(HIV-1)} in Thailand, we determined proviral sequences for 63 {HIV-1-infected} patients in various risk groups from all over the country between April and July, 1991.  Two distinct genotypes of {HIV-1,} A and B, were found to segregate by mode of transmission. Of 29 sexually infected patients, 25 (86\%) had {HIV-1} of genotype A and 4 (14\%) had genotype B. Among 29 injecting drug users, probably parenterally infected, only 7 (24\%) had genotype A and 22 (76\%) had genotype B. This segregation is unlikely to have arisen by chance (p{\textless}0�001). No patient was found to have dual infection. Nucleotide divergence averaged 3�4\% among {genotype-A-infected} patients and 3�5\% among {genotype-B-infected} patients, but 22�0\% between the genotypes. 37 of 40 isolates (both genotypes) had the G {PGQ} tetrapeptide at the tip of the V3 loop, which is common in African {HIV-1} strains but rare in North American and European strains, where the {GPGR} motif predominates.  These findings suggest that the waves of {HIV-1} infection in injecting drug users and in sexually infected patients in Thailand may not be epidemiologically linked. The nucleotide divergence data point to the separate introductions of the two genotypes into Thailand. Further studies in Thailand and neighbouring countries will be useful in the design and selection of candidate {HIV} vaccines.},  Author = {Ou, C. {-Y.} and Weniger, B. G. and Luo, C. {-C.} and Kalish, M. L. and Gayle, H. D. and Young, N. L. and Schochetman, G. and Takebe, Y. and Yamazaki, S. and Auwanit, W.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1016/0140-6736(93)91001-3},  Issn = {0140-6736},  Journal = {The Lancet},  Month = may,  Number = {8854},  Pages = {1171--1174},  Title = {Independent introduction of two major {HIV-1} genotypes into distinct high-risk populations in Thailand},  Url = {http://www.sciencedirect.com/science/article/B6T1B-49KCHRT-TN/2/eaf0713e440789839be3552d4ba6f359},  Volume = {341},  Year = {1993},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6T1B-49KCHRT-TN/2/eaf0713e440789839be3552d4ba6f359},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/0140-6736(93)91001-3}}  @misc{p.:a.h.,  Annote = {Nature Publishing Group Metadata Repository  [http://www.nature.com/oai/request] {(Switzerland)}  {ER}},  Author = {Sneath, P. H. A. and Sokal, Robert R.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Month = mar,  Publisher = {Nature Publishing Group},  Title = {Numerical Taxonomy},  Year = {1962}}  @article{Page:2002if,  Abstract = {Darwinian evolution is based on three fundamental principles, reproduction, mutation and selection, which describe how populations change over time and how new forms evolve out of old ones. There are numerous mathematical descriptions of the resulting evolutionary dynamics. In this paper, we show that apparently very different formulations are part of a single unified framework. At the center of this framework is the equivalence between the replicator-mutator equation and the Price equation. From these equations, we obtain as special cases adaptive dynamics, evolutionary game dynamics, the Lotka-Volterra equation of ecology and the quasispecies equation of molecular evolution.},  Author = {Page, Karen M and Nowak, Martin A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {J Theor Biol},  Journal-Full = {Journal of theoretical biology},  Mesh = {Animals; Evolution; Models, Genetic; Population Dynamics; Reproduction; Selection, Genetic},  Month = {Nov},  Number = {1},  Pages = {93-8},  Pmid = {12392978},  Pst = {ppublish},  Title = {Unifying evolutionary dynamics},  Volume = {219},  Year = {2002}}  @article{paraskevis:2005sl,  Abstract = {Summary: We developed a software tool {(SlidingBayes)} for recombination analysis based on Bayesian phylogenetic inference. {Sliding-Bayes} provides a powerful approach for detecting potential recombination, especially between highly divergent sequences and complex {HIV-1} recombinants for which simpler methods like neighbor joining {(NJ)} may be less powerful. {SlidingBayes} guides Markov Chain Monte Carlo {(MCMC)} sampling performed by {MrBayes} in a sliding window across the alignment {(Bayesian} scanning). The tool can be used for nucleotide and amino acid sequences and combines all the modeling possibilities of {MrBayes} with the ability to plot the posterior probability support for clustering of various combinations of taxa. Availability: {SlidingBayes} is available at {http://www.kuleuven.ac.be/rega/cev/Software/} Contact: [email protected] Supplementary information: A quick guide and examples for {SlidingBayes} are available at {http://www.kuleuven.ac.be/rega/cev/Software/}},  Author = {Paraskevis, D. and Deforche, K. and Lemey, P. and Magiorkinis, G. and Hatzakis, A. and Vandamme, {A.-M.}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/bioinformatics/bti139},  Journal = {Bioinformatics},  Number = {7},  Pages = {1274--1275},  Title = {{SlidingBayes:} exploring recombination using a sliding window approach based on Bayesian phylogenetic inference},  Url = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/21/7/1274},  Volume = {21},  Year = {2005},  Bdsk-Url-1 = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/21/7/1274},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/bioinformatics/bti139}}  @article{Parker:2008ye,  Abstract = {Many recent studies have sought to quantify the degree to which viral phenotypic characters (such as epidemiological risk group, geographic location, cell tropism, drug resistance state, etc.) are correlated with shared ancestry, as represented by a viral phylogenetic tree. Here, we present a new Bayesian Markov-Chain Monte Carlo approach to the investigation of such phylogeny-trait correlations. This method accounts for uncertainty arising from phylogenetic error and provides a statistical significance test of the null hypothesis that traits are associated randomly with phylogeny tips. We perform extensive simulations to explore and compare the behaviour of three statistics of phylogeny-trait correlation. Finally, we re-analyse two existing published data sets as case studies. Our framework aims to provide an improvement over existing methods for this problem.},  Author = {Parker, Joe and Rambaut, Andrew and Pybus, Oliver G},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.meegid.2007.08.001},  Journal = {Infect Genet Evol},  Journal-Full = {Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases},  Mesh = {Algorithms; Computer Simulation; Data Interpretation, Statistical; Empirical Research; Phenotype; Phylogeny; Uncertainty; Virus Physiological Phenomena; Viruses},  Month = {May},  Number = {3},  Pages = {239-46},  Pmid = {17921073},  Pst = {ppublish},  Title = {Correlating viral phenotypes with phylogeny: accounting for phylogenetic uncertainty},  Volume = {8},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.meegid.2007.08.001}}  @article{parrish:2008cr,  Abstract = {Summary: Host range is a viral property reflecting natural hosts that are infected either as part of a principal transmission cycle or, less commonly, as "spillover" infections into alternative hosts. Rarely, viruses gain the ability to spread efficiently within a new host that was not previously exposed or susceptible. These transfers involve either increased exposure or the acquisition of variations that allow them to overcome barriers to infection of the new hosts. In these cases, devastating outbreaks can result. Steps involved in transfers of viruses to new hosts include contact between the virus and the host, infection of an initial individual leading to amplification and an outbreak, and the generation within the original or new host of viral variants that have the ability to spread efficiently between individuals in populations of the new host. Here we review what is known about host switching leading to viral emergence from known examples, considering the evolutionary mechanisms, virus-host interactions, host range barriers to infection, and processes that allow efficient host-to-host transmission in the new host population.},  Author = {Parrish, Colin R. and Holmes, Edward C. and Morens, David M. and Park, {Eun-Chung} and Burke, Donald S. and Calisher, Charles H. and Laughlin, Catherine A. and Saif, Linda J. and Daszak, Peter},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/MMBR.00004-08},  Journal = {Microbiology and Molecular Biology Reviews},  Month = sep,  Number = {3},  Pages = {457--470},  Title = {{Cross-Species} Virus Transmission and the Emergence of New Epidemic Diseases},  Url = {http://mmbr.asm.org/cgi/content/abstract/72/3/457},  Volume = {72},  Year = {2008},  Bdsk-Url-1 = {http://mmbr.asm.org/cgi/content/abstract/72/3/457},  Bdsk-Url-2 = {http://dx.doi.org/10.1128/MMBR.00004-08}}  @article{Parsons:2007vn,  Abstract = {We extend the one-locus two allele Moran model of fixation in a haploid population to the case where the total size of the population is not fixed. The model is defined as a two-dimensional birth-and-death process for allele number. Changes in allele number occur through density-independent death events and birth events whose per capita rate decreases linearly with the total population density. Uniquely for models of this type, the latter is determined by these same birth-and-death events. This provides a framework for investigating both the effects of fluctuation in total population number through demographic stochasticity, and deterministic density-dependent changes in mean density, on allele fixation. We analyze this model using a combination of asymptotic analytic approximations supported by numerics. We find that for advantageous mutants demographic stochasticity of the resident population does not affect the fixation probability, but that deterministic changes in total density do. In contrast, for deleterious mutants, the fixation probability increases with increasing resident population fluctuation size, but is relatively insensitive to initial density. These phenomena cannot be described by simply using a harmonic mean effective population size.},  Author = {Parsons, Todd L and Quince, Christopher},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.tpb.2006.11.004},  Journal = {Theor Popul Biol},  Journal-Full = {Theoretical population biology},  Mesh = {Alleles; Genetics, Population; Haploidy; Logistic Models; Markov Chains; Models, Genetic; Mutation; Population Density; Stochastic Processes},  Month = {Aug},  Number = {1},  Pages = {121-35},  Pmid = {17239910},  Pst = {ppublish},  Title = {Fixation in haploid populations exhibiting density dependence I: The non-neutral case},  Volume = {72},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tpb.2006.11.004}}  @article{Parsons:2010fk,  Abstract = {Much of population genetics is based on the diffusion limit of the Wright-Fisher model, which assumes a fixed population size. This assumption is violated in most natural populations, particularly for microbes. Here we study a more realistic model that decouples birth and death events and allows for a stochastically varying population size. Under this model, classical quantities such as the probability of and time before fixation of a mutant allele can differ dramatically from their Wright-Fisher expectations. Moreover, inferences about natural selection based on Wright-Fisher assumptions can yield erroneous and even contradictory conclusions: at small population densities one allele will appear superior, whereas at large densities the other allele will dominate. Consequently, competition assays in laboratory conditions may not reflect the outcome of long-term evolution in the field. These results highlight the importance of incorporating demographic stochasticity into basic models of population genetics.},  Author = {Parsons, Todd L and Quince, Christopher and Plotkin, Joshua B},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1534/genetics.110.115030},  Journal = {Genetics},  Journal-Full = {Genetics},  Month = {Aug},  Number = {4},  Pages = {1345-54},  Pmc = {PMC2927761},  Pmid = {20457879},  Pst = {ppublish},  Title = {Some consequences of demographic stochasticity in population genetics},  Volume = {185},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.110.115030}}  @article{Perelson:1996qf,  Abstract = {A new mathematical model was used to analyze a detailed set of human immunodeficiency virus-type 1 (HIV-1) viral load data collected from five infected individuals after the administration of a potent inhibitor of HIV-1 protease. Productively infected cells were estimated to have, on average, a life-span of 2.2 days (half-life t 1/2 = 1.6 days), and plasma virions were estimated to have a mean life-span of 0.3 days (t 1/2 = 0.24 days). The estimated average total HIV-1 production was 10.3 x 10(9) virions per day, which is substantially greater than previous minimum estimates. The results also suggest that the minimum duration of the HIV-1 life cycle in vivo is 1.2 days on average, and that the average HIV-1 generation time--defined as the time from release of a virion until it infects another cell and causes the release of a new generation of viral particles--is 2.6 days. These findings on viral dynamics provide not only a kinetic picture of HIV-1 pathogenesis, but also theoretical principles to guide the development of treatment strategies.},  Author = {Perelson, A S and Neumann, A U and Markowitz, M and Leonard, J M and Ho, D D},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Antiviral Agents; CD4 Lymphocyte Count; CD4-Positive T-Lymphocytes; Cell Survival; HIV Infections; HIV Protease Inhibitors; HIV-1; Half-Life; Humans; Kinetics; Models, Biological; RNA, Viral; Regression Analysis; Ritonavir; Thiazoles; Valine; Viremia; Virion; Virus Replication},  Month = {Mar},  Number = {5255},  Pages = {1582-6},  Pmid = {8599114},  Pst = {ppublish},  Title = {HIV-1 dynamics in vivo: virion clearance rate, infected cell life-span, and viral generation time},  Volume = {271},  Year = {1996}}  @article{pond:2008es,  Abstract = {Human immunodeficiency virus {(HIV-1)} can rapidly evolve due to selection pressures exerted by {HIV-specific} immune responses, antiviral agents, and to allow the virus to establish infection in different compartments in the body. Statistical models applied to {HIV-1} sequence data can help to elucidate the nature of these selection pressures through comparisons of non-synonymous (or amino acid changing) and synonymous (or amino acid preserving) substitution rates. These models also need to take into account the non-independence of sequences due to their shared evolutionary history. We review how we have developed these methods and have applied them to characterize the evolution of {HIV-1} in vivo. To illustrate our methods, we present an analysis of compartment-specific evolution of {HIV-1} env in blood and cerebrospinal fluid and of site-to-site variation in the gag gene of subtype C {HIV-1.} Copyright {\copyright} 2008 John Wiley \& Sons, Ltd.},  Author = {Pond, S. L. Kosakovsky and Poon, A. F. Y. and Z{\'a}rate, S. and Smith, D. M. and Little, S. J. and Pillai, S. K. and Ellis, R. J. and Wong, J. K. and Brown, A. J. Leigh and Richman, D. D. and Frost, S. D. W.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1002/sim.3192},  Journal = {Statistics in Medicine},  Number = {23},  Pages = {4779--4789},  Title = {Estimating selection pressures on {HIV-1} using phylogenetic likelihood models},  Url = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1002/sim.3192},  Volume = {27},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1002/sim.3192},  Bdsk-Url-2 = {http://dx.doi.org/10.1002/sim.3192}}  @article{Pybus:2007ly,  Abstract = {Populations of RNA viruses are often characterized by abundant genetic variation. However, the relative fitness of these mutations is largely unknown, although this information is central to our understanding of viral emergence, immune evasion, and drug resistance. Here we develop a phylogenetic method, based on the distribution of nonsynonymous and synonymous changes, to assess the relative fitness of polymorphisms in the structural genes of 143 RNA viruses. This reveals that a substantial proportion of the amino acid variation observed in natural populations of RNA viruses comprises transient deleterious mutations that are later purged by purifying selection, potentially limiting virus adaptability. We also demonstrate, for the first time, the existence of a relationship between amino acid variability and the phylogenetic distribution of polymorphisms. From this relationship, we propose an empirical threshold for the maximum viable deleterious mutation load in RNA viruses.},  Author = {Pybus, Oliver G and Rambaut, Andrew and Belshaw, Robert and Freckleton, Robert P and Drummond, Alexei J and Holmes, Edward C},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1093/molbev/msm001},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Amino Acid Sequence; Computational Biology; Evolution, Molecular; Likelihood Functions; Models, Genetic; Mutation; Phylogeny; Polymorphism, Genetic; RNA Viruses; Selection, Genetic},  Month = {Mar},  Number = {3},  Pages = {845-52},  Pmid = {17218639},  Pst = {ppublish},  Title = {Phylogenetic evidence for deleterious mutation load in RNA viruses and its contribution to viral evolution},  Volume = {24},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msm001}}  @article{Pybus:2007tw,  Abstract = {The hepatitis C virus (HCV) infects at least 3\% of people worldwide and is a leading global cause of liver disease. Although HCV spread epidemically during the 20th century, particularly by blood transfusion, it has clearly been present in human populations for several centuries. Here we attempt to redress the paucity of investigation into how long-term endemic transmission of HCV has been maintained. Such transmission not only represents the 'natural' route of infection but also contributes to new infections today. As a first step, we investigate the hypothesis that HCV can be mechanically transmitted by biting arthropods. Firstly, we use a combined bioinformatic and geographic approach to build a spatial database of endemic HCV infection and demonstrate that this can be used to geographically compare endemic HCV with the range distributions of potential vector species. Second, we use models from mathematical epidemiology to investigate if the parameters that describe the biting behaviour of vectors are consistent with a proposed basic reproduction number (R0) for HCV, and with the sustained transmission of the virus by mechanical transmission. Our analyses indicate that the mechanical transmission of HCV is plausible and that much further research into endemic HCV is needed.},  Author = {Pybus, Oliver G and Markov, Peter V and Wu, Anna and Tatem, Andrew J},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.ijpara.2007.04.009},  Journal = {Int J Parasitol},  Journal-Full = {International journal for parasitology},  Mesh = {Animals; Culicidae; Endemic Diseases; Hepacivirus; Hepatitis C; Humans; Insect Vectors; Models, Biological; Prevalence; World Health},  Month = {Jul},  Number = {8-9},  Pages = {839-49},  Pmid = {17521655},  Pst = {ppublish},  Title = {Investigating the endemic transmission of the hepatitis C virus},  Volume = {37},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ijpara.2007.04.009}}  @article{Pybus:2009fu,  Abstract = {The hepatitis C virus (HCV), which currently infects an estimated 3\% of people worldwide, has been present in some human populations for several centuries, notably HCV genotypes 1 and 2 in West Africa and genotype 6 in Southeast Asia. Here we use newly developed methods of sequence analysis to conduct the first comprehensive investigation of the epidemic and evolutionary history of HCV in Asia. Our analysis includes new HCV core (n = 16) and NS5B (n = 14) gene sequences, obtained from serum samples of jaundiced patients from Laos. These exceptionally diverse isolates were analyzed in conjunction with all available reference strains using phylogenetic and Bayesian coalescent methods. We performed statistical tests of phylogeographic structure and applied a recently developed "relaxed molecular clock" approach to HCV for the first time, which indicated an unexpectedly high degree of rate variation. Our results reveal a >1,000-year-long development of genotype 6 in Asia, characterized by substantial phylogeographic structure and two distinct phases of epidemic history, before and during the 20th century. We conclude that HCV lineages representing preexisting and spatially restricted strains were involved in multiple, independent local epidemics during the 20th century. Our analysis explains the generation and maintenance of HCV diversity in Asia and could provide a template for further investigations of HCV spread in other regions.},  Author = {Pybus, Oliver G and Barnes, Eleanor and Taggart, Rachel and Lemey, Philippe and Markov, Peter V and Rasachak, Bouachan and Syhavong, Bounkong and Phetsouvanah, Rattanaphone and Sheridan, Isabelle and Humphreys, Isla S and Lu, Ling and Newton, Paul N and Klenerman, Paul},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:57:31 +0000},  Doi = {10.1128/JVI.01501-08},  Journal = {J Virol},  Journal-Full = {Journal of virology},  Mesh = {Evolution, Molecular; Far East; Hepacivirus; Hepatitis C; Molecular Epidemiology; Phylogeny; Sequence Analysis, DNA; Time Factors; Viral Core Proteins; Viral Nonstructural Proteins},  Month = {1},  Number = {2},  Pages = {1071-82},  Pmc = {PMC2612398},  Pmid = {18971279},  Pst = {ppublish},  Title = {Genetic history of hepatitis C virus in East Asia},  Volume = {83},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.01501-08}}  @article{Pybus:2009ys,  Abstract = {Many organisms that cause infectious diseases, particularly RNA viruses, mutate so rapidly that their evolutionary and ecological behaviours are inextricably linked. Consequently, aspects of the transmission and epidemiology of these pathogens are imprinted on the genetic diversity of their genomes. Large-scale empirical analyses of the evolutionary dynamics of important pathogens are now feasible owing to the increasing availability of pathogen sequence data and the development of new computational and statistical methods of analysis. In this Review, we outline the questions that can be answered using viral evolutionary analysis across a wide range of biological scales.},  Author = {Pybus, Oliver G and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nrg2583},  Journal = {Nat Rev Genet},  Journal-Full = {Nature reviews. Genetics},  Mesh = {Animals; Communicable Diseases; Evolution, Molecular; Humans; RNA Viruses; Virus Diseases},  Month = {Aug},  Number = {8},  Pages = {540-50},  Pmid = {19564871},  Pst = {ppublish},  Title = {Evolutionary analysis of the dynamics of viral infectious disease},  Volume = {10},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nrg2583}}  @article{Rambaut:2000zt,  Abstract = {MOTIVATION: TipDate is a program that will use sequences that have been isolated at different dates to estimate their rate of molecular evolution. The program provides a maximum likelihood estimate of the rate and also the associated date of the most recent common ancestor of the sequences, under a model which assumes a constant rate of substitution (molecular clock) but which accommodates the dates of isolation. Confidence intervals for these parameters are also estimated. RESULTS: The approach was applied to a sample of 17 dengue virus serotype 4 sequences, isolated at dates ranging from 1956 to 1994. The rate of substitution for this serotype was estimated to be 7.91 x 10(-4) substitutions per site per year (95\% confidence intervals of 6.07 x 10(-4), 9.86 x 10(-4)). This is compatible with a date of 1922 (95\% confidence intervals of 1900-1936) for the most recent common ancestor of these sequences. AVAILABILITY: TipDate can be obtained by WWW from http://evolve.zoo. ox.ac.uk/software. The package includes the source code, manual and example files. Both UNIX and Apple Macintosh versions are available from the same site.},  Author = {Rambaut, A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Bioinformatics},  Journal-Full = {Bioinformatics (Oxford, England)},  Mesh = {DNA, Viral; Dengue Virus; Evolution, Molecular; Humans; Likelihood Functions; Phylogeny; Sequence Analysis, DNA; Software; Viral Envelope Proteins},  Month = {Apr},  Number = {4},  Pages = {395-9},  Pmid = {10869038},  Pst = {ppublish},  Title = {Estimating the rate of molecular evolution: incorporating non-contemporaneous sequences into maximum likelihood phylogenies},  Volume = {16},  Year = {2000}}  @article{rambaut:2004ca,  Annote = {10.1038/nrg1246},  Author = {Rambaut, Andrew and Posada, David and Crandall, Keith A. and Holmes, Edward C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nrg1246},  Issn = {1471-0056},  Journal = {Nat Rev Genet},  Month = jan,  Number = {1},  Pages = {52--61},  Title = {The causes and consequences of {HIV} evolution},  Url = {http://dx.doi.org/10.1038/nrg1246},  Volume = {5},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nrg1246}}  @article{Rambaut:2008kl,  Abstract = {The evolutionary interaction between influenza A virus and the human immune system, manifest as 'antigenic drift' of the viral haemagglutinin, is one of the best described patterns in molecular evolution. However, little is known about the genome-scale evolutionary dynamics of this pathogen. Similarly, how genomic processes relate to global influenza epidemiology, in which the A/H3N2 and A/H1N1 subtypes co-circulate, is poorly understood. Here through an analysis of 1,302 complete viral genomes sampled from temperate populations in both hemispheres, we show that the genomic evolution of influenza A virus is characterized by a complex interplay between frequent reassortment and periodic selective sweeps. The A/H3N2 and A/H1N1 subtypes exhibit different evolutionary dynamics, with diverse lineages circulating in A/H1N1, indicative of weaker antigenic drift. These results suggest a sink-source model of viral ecology in which new lineages are seeded from a persistent influenza reservoir, which we hypothesize to be located in the tropics, to sink populations in temperate regions.},  Author = {Rambaut, Andrew and Pybus, Oliver G and Nelson, Martha I and Viboud, Cecile and Taubenberger, Jeffery K and Holmes, Edward C},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nature06945},  Journal = {Nature},  Journal-Full = {Nature},  Mesh = {Evolution, Molecular; Genetic Drift; Genetic Variation; Genome, Viral; Hemagglutinin Glycoproteins, Influenza Virus; Humans; Influenza A Virus, H1N1 Subtype; Influenza A Virus, H3N2 Subtype; Influenza, Human; Models, Biological; Neuraminidase; New York; New Zealand; Phylogeny; Reassortant Viruses},  Month = {May},  Number = {7195},  Pages = {615-9},  Pmc = {PMC2441973},  Pmid = {18418375},  Pst = {ppublish},  Title = {The genomic and epidemiological dynamics of human influenza A virus},  Volume = {453},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature06945}}  @article{Rambaut:2009dz,  Abstract = {Swine-origin pandemic human influenza A virus (H1N1pdm) has spread rapidly around the world since its initial documentation in April 2009. Here we have updated initial estimates of the rate of molecular evolution and estimates of the time of origin of this virus in the human population using the large number of viral sequences made available as part of the public health response to this global pandemic. Currently sampled H1N1pdm sequences share a most recent common ancestor in the first 7 weeks of 2009 with the implication that the virus was transmitting cryptically for up to 3 months prior to recognition. A phylogenetic reconstruction of the data shows that the virus has been circling the globe extensively with multiple introductions into most geographical areas.},  Author = {Rambaut, Andrew and Holmes, Edward C.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 03:56:47 +0000},  Journal = {PLoS Curr Influenza},  Journal-Full = {PLoS currents. Influenza},  Pages = {RRN1003},  Pmc = {PMC2762654},  Pmid = {20025195},  Pst = {epublish},  Title = {The early molecular epidemiology of the swine-origin A/H1N1 human influenza pandemic},  Year = {2009}}  @article{reid:1999or,  Abstract = {The {"Spanish"} influenza pandemic killed over 20 million people in 1918 and 1919, making it the worst infectious pandemic in history. Here, we report the complete sequence of the hemagglutinin {(HA)} gene of the 1918 virus. Influenza {RNA} for the analysis was isolated from a formalin-fixed, paraffin-embedded lung tissue sample prepared during the autopsy of a victim of the influenza pandemic in 1918. Influenza {RNA} was also isolated from lung tissue samples from two additional victims of the lethal 1918 influenza: one formalin-fixed, paraffin-embedded sample and one frozen sample obtained by in situ biopsy of the lung of a victim buried in permafrost since 1918. The complete coding sequence of the {A/South} Carolina/1/18 {HA} gene was obtained. The {HA1} domain sequence was confirmed by using the two additional isolates {(A/New} York/1/18 and {A/Brevig} Mission/1/18). The sequences show little variation. Phylogenetic analyses suggest that the 1918 virus {HA} gene, although more closely related to avian strains than any other mammalian sequence, is mammalian and may have been adapting in humans before 1918.},  Author = {Reid, A H and Fanning, T G and Hultin, J V and Taubenberger, J K},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0027-8424},  Journal = {Proceedings of the National Academy of Sciences of the United States of America},  Keywords = {Adult, Amino Acid Sequence, Base Sequence, Evolution, Molecular, Hemagglutinin Glycoproteins, Influenza Virus, History, 20th Century, Humans, Influenza A virus, Influenza, Human, Male, Molecular Sequence Data, Phylogeny},  Month = feb,  Note = {{PMID:} 9990079},  Number = {4},  Pages = {1651--1656},  Title = {Origin and evolution of the 1918 {"Spanish"} influenza virus hemagglutinin gene},  Url = {http://www.ncbi.nlm.nih.gov/pubmed/9990079},  Volume = {96},  Year = {1999},  Bdsk-Url-1 = {http://www.ncbi.nlm.nih.gov/pubmed/9990079}}  @article{reis:2009us,  Author = {Reis, Mario and Hay, Alan J. and Goldstein, Richard A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1007/s00239-009-9282-x},  Issn = {0022-2844},  Journal = {Journal of Molecular Evolution},  Number = {4},  Pages = {333--345},  Title = {Using {Non-Homogeneous} Models of Nucleotide Substitution to Identify Host Shift Events: Application to the Origin of the 1918 {`Spanish'} Influenza Pandemic Virus},  Url = {http://www.springerlink.com/index/10.1007/s00239-009-9282-x},  Volume = {69},  Year = {2009},  Bdsk-Url-1 = {http://www.springerlink.com/index/10.1007/s00239-009-9282-x},  Bdsk-Url-2 = {http://dx.doi.org/10.1007/s00239-009-9282-x}}  @article{resik:2007li,  Abstract = {Sequence analysis can be used to evaluate transmission networks. We have used retrospective samples to examine two {HIV-1} transmission networks established by contact tracing. Regions of the {HIV-1} region representing segments of gag and env were amplified by {RT-PCR} from frozen plasma samples and the sequence of each {PCR} product was determined. Within one of the networks (composed of 38 subjects) we found only a subset of the tested sequence clusters was consistent with the reported epidemiological linkage. Of 15 presumed transmission events where sequence data were available, 9 could be rejected either by subtype mismatch or by phylogenetic tests. In the other network (composed of 89 subjects) we were able to assess sequences for 26 presumed transmission events, 18 of which were rejected based on subtype discordance. Long lags in time between the time of transmission and the time of sequence sampling (ranging from 2 to 18 years) may limit the sensitivity for the detection of sequence linkage. Also, superinfection and incomplete epidemiological information are other factors that will limit the concordance of phylogenetic reconstruction and reported epidemiological linkage.},  Annote = {doi: 10.1089/aid.2006.0158},  Author = {Resik, Sonia and Lemey, Philippe and Ping, {Li-Hua} and Kouri, Vivian and Joanes, Jose and P{\'e}rez, Jorge and Vandamme, {Anne-Mieke} and Swanstrom, Ronald},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {{AIDS} Research and Human Retroviruses},  Month = mar,  Number = {3},  Pages = {347--356},  Title = {Limitations to Contact Tracing And Phylogenetic Analysis in Establishing {HIV} Type 1 Transmission Networks in Cuba},  Url = {http://dx.doi.org/10.1089/aid.2006.0158},  Volume = {23},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1089/aid.2006.0158}}  @article{rest:2003sa,  Annote = {The sudden appearance and potential lethality of severe acute respiratory syndrome associated coronavirus {(SARS-CoV)} in humans has focused attention on understanding its origins. Here, we assess phylogenetic relationships for the {SARS-CoV} lineage as well as the history of host-species shifts for {SARS-CoV} and other coronaviruses. We used a Bayesian phylogenetic inference approach with sliding window analyses of three {SARS-CoV} proteins: {RNA} dependent {RNA} polymerase {(RDRP),} nucleocapsid {(N)} and spike {(S).} Conservation of {RDRP} allowed us to use a set of Arteriviridae taxa to root the Coronaviridae phylogeny. We found strong evidence for a recombination breakpoint within {SARS-CoV} {RDRP,} based on different, well supported trees for a 5' fragment (supporting {SARS-CoV} as sister to a clade including all other coronaviruses) and a 3' fragment (supporting {SARS-CoV} as sister to group three avian coronaviruses). These different topologies are statistically significant: the optimal 5' tree could be rejected for the 3' region, and the optimal 3' tree could be rejected for the 5' region. We did not find statistical evidence for recombination in analyses of N and S, as there is little signal to differentiate among alternative trees. Comparison of phylogenetic trees for 11 known host-species and 36 coronaviruses, representing coronavirus groups 1-3 and {SARS-CoV,} based on N showed statistical incongruence indicating multiple host-species shifts for coronaviruses. Inference of host-species associations is highly sensitive to sampling and must be considered cautiously. However, current sampling suggests host-species shifts between mouse and rat, chicken and turkey, mammals and manx shearwater, and humans and other mammals. The sister relationship between avian coronaviruses and the 3' {RDRP} fragment of {SARS-CoV} suggests an additional host-species shift. Demonstration of recombination in the {SARS-CoV} lineage indicates its potential for rapid unpredictable change, a potentially important challenge for public health management and for drug and vaccine development.},  Author = {Rest, Joshua S. and Mindell, David P.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1016/j.meegid.2003.08.001},  Issn = {1567-1348},  Journal = {Infection, Genetics and Evolution},  Keywords = {Coronavirus, Host-shift, Phylogeny, recombination, {RNA-dependent} {RNA} polymerase, {SARS-CoV} Nidovirales, Severe acute respiratory syndrome},  Number = {3},  Pages = {219--225},  Title = {{SARS} associated coronavirus has a recombinant polymerase and coronaviruses have a history of host-shifting},  Url = {http://www.sciencedirect.com/science/article/B6W8B-49H6WPK-1/2/e60c85a7466119e9978b4238e8d52260},  Volume = {3},  Year = {2003},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6W8B-49H6WPK-1/2/e60c85a7466119e9978b4238e8d52260},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.meegid.2003.08.001}}  @article{rios:2007an,  Abstract = {This study reports the analysis of human immunodeficiency virus type 1 {(HIV-1)} protease {(PR)} and reverse transcriptase {(RT)} coding sequences from 136 {HIV-1-infected} subjects from Chile, 66 (49\%) of them under antiretroviral {(ARV)} treatment. The prevalence of mutations conferring high or intermediate resistance levels to {ARVs} was 77\% among treated patients and 2.5\% among drug-na{\"\i}ve subjects. The distribution of resistance prevalence in treated patients by drug class was 61\% to nucleoside {RT} inhibitors, 84\% to nonnucleoside {RT} inhibitors, and 46\% to {PR} inhibitors. Phylogenetic analysis revealed that 115 (85\%) subjects were infected with subtype B viruses, 1 with a subtype F1 virus, and 20 (15\%) carried {BF} intersubtype recombinants. Most {BF} recombinants grouped into two clusters, one related to {CRF12\_BF,} while the other could represent a new circulating recombinant form {(CRF).} In conclusion, this is the first report analysing the prevalence of {ARV} resistance which includes patients under {HAART} from Chile. Additionally, phylogenetic analysis of the {PR-RT} coding sequences reveals the presence of {BF} intersubtype recombinants. J. Med. Virol. 79: 647-656, 2007. {\copyright} 2007 {Wiley-Liss,} Inc.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1002/jmv.20881},  Journal = {Journal of Medical Virology},  Number = {6},  Pages = {647--656},  Title = {Antiretroviral drug resistance and phylogenetic diversity of {HIV-1} in Chile},  Url = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1002/jmv.20881},  Volume = {79},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1002/jmv.20881},  Bdsk-Url-2 = {http://dx.doi.org/10.1002/jmv.20881}}  @article{Roberts:2007fk,  Abstract = {The concept of the basic reproduction number (R0) occupies a central place in epidemic theory. The value of R0 determines the proportion of the population that becomes infected over the course of a (modelled) epidemic. In many models, (i) an endemic infection can persist only if R0>1, (ii) the value of R0 provides a direct measure of the control effort required to eliminate the infection, and (iii) pathogens evolve to maximize their value of R0. These three statements are not universally true. In this paper, some exceptions to them are discussed, based on the extensions of the SIR model.},  Author = {Roberts, M G},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1098/rsif.2007.1031},  Journal = {J R Soc Interface},  Journal-Full = {Journal of the Royal Society, Interface / the Royal Society},  Mesh = {Animal Diseases; Animals; Animals, Wild; Communicable Diseases; Disease Transmission, Infectious; Models, Biological; Models, Statistical},  Month = {Oct},  Number = {16},  Pages = {949-61},  Pmc = {PMC2075534},  Pmid = {17490942},  Pst = {ppublish},  Title = {The pluses and minuses of R0},  Volume = {4},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rsif.2007.1031}}  @article{robertson:1995:re,  Author = {Robertson, David L. and Hahn, Beatrice H. and Sharp, Paul M.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1007/BF00163230},  Issn = {0022-2844},  Journal = {Journal of Molecular Evolution},  Number = {3},  Pages = {249--259},  Title = {Recombination in {AIDS} viruses},  Url = {http://www.springerlink.com.ezproxy.auckland.ac.nz/content/v3255733652v8848/},  Volume = {40},  Year = {1995},  Bdsk-Url-1 = {http://www.springerlink.com.ezproxy.auckland.ac.nz/content/v3255733652v8848/},  Bdsk-Url-2 = {http://dx.doi.org/10.1007/BF00163230}}  @article{Rodrigo_etal:1999,  Abstract = {The generation time of HIV Type 1 (HIV-1) in vivo has previously been estimated using a mathematical model of viral dynamics and was found to be on the order of one to two days per generation. Here, we describe a new method based on coalescence theory that allows the estimate of generation times to be derived by using nucleotide sequence data and a reconstructed genealogy of sequences obtained over time. The method is applied to sequences obtained from a long-term nonprogressing individual at five sampling occasions. The estimate of viral generation time using the coalescent method is 1.2 days per generation and is close to that obtained by mathematical modeling (1.8 days per generation), thus strengthening confidence in estimates of a short viral generation time. Apart from the estimation of relevant parameters relating to viral dynamics, coalescent modeling also allows us to simulate the evolutionary behavior of samples of sequences obtained over time.},  Author = {Rodrigo, A. G. and Shpaer, E G and Delwart, E L and Iversen, A K and Gallo, M V and Brojatsch, J and Hirsch, M S and Walker, B D and Mullins, J I},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 01:02:27 +0000},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {DNA, Viral; Evolution, Molecular; Genes, env; HIV Seropositivity; HIV-1; Homosexuality, Male; Humans; Male; Models, Genetic; Models, Statistical; Molecular Sequence Data; Phylogeny; Time Factors; Virus Replication},  Month = {3},  Number = {5},  Pages = {2187-91},  Pmc = {PMC26758},  Pmid = {10051616},  Pst = {ppublish},  Title = {Coalescent estimates of HIV-1 generation time in vivo},  Volume = {96},  Year = {1999}}  @article{Rouzine:1999fk,  Abstract = {The effective size of the HIV population in vivo, although critically important for the prediction of appearance of drug-resistant variants, is currently unknown. To address this issue, we have developed a simple virus population model, within which the relative importance of stochastic factors and purifying selection for genetic evolution differs over, at least, three broad intervals of the effective population size, with approximate boundaries given by the inverse selection coefficient and the inverse mutation rate per base per cycle. Random drift and selection dominate the smallest (stochastic) and largest (deterministic) population intervals, respectively. In the intermediate (selection-drift) interval, random drift controls weakly diverse populations, whereas strongly diverse populations are controlled by selection. To estimate the effective size of the HIV population in vivo, we tested 200 pro sequences isolated from 11 HIV-infected patients for the presence of a linkage disequilibrium effect which must exist only in small populations. This analysis demonstrated a steady-state virus population of 10(5) infected cells or more, which is either in or at the border of the deterministic regime with respect to evolution of separate bases.},  Author = {Rouzine, I M and Coffin, J M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Computer Simulation; Evolution, Molecular; Gene Products, env; Genome, Viral; HIV; Haplotypes; Linkage Disequilibrium; Models, Genetic; Monte Carlo Method; Mutation; Stochastic Processes; Time Factors},  Month = {Sep},  Number = {19},  Pages = {10758-63},  Pmc = {PMC17956},  Pmid = {10485899},  Pst = {ppublish},  Title = {Linkage disequilibrium test implies a large effective population number for HIV in vivo},  Volume = {96},  Year = {1999}}  @article{Rouzine:2001zr,  Abstract = {We present here a self-contained analytic review of the role of stochastic factors acting on a virus population. We develop a simple one-locus, two-allele model of a haploid population of constant size including the factors of random drift, purifying selection, and random mutation. We consider different virological experiments: accumulation and reversion of deleterious mutations, competition between mutant and wild-type viruses, gene fixation, mutation frequencies at the steady state, divergence of two populations split from one population, and genetic turnover within a single population. In the first part of the review, we present all principal results in qualitative terms and illustrate them with examples obtained by computer simulation. In the second part, we derive the results formally from a diffusion equation of the Wright-Fisher type and boundary conditions, all derived from the first principles for the virus population model. We show that the leading factors and observable behavior of evolution differ significantly in three broad intervals of population size, N. The "neutral limit" is reached when N is smaller than the inverse selection coefficient. When N is larger than the inverse mutation rate per base, selection dominates and evolution is "almost" deterministic. If the selection coefficient is much larger than the mutation rate, there exists a broad interval of population sizes, in which weakly diverse populations are almost neutral while highly diverse populations are controlled by selection pressure. We discuss in detail the application of our results to human immunodeficiency virus population in vivo, sampling effects, and limitations of the model.},  Author = {Rouzine, I M and Rodrigo, A. G. and Coffin, J M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 01:00:31 +0000},  Doi = {10.1128/MMBR.65.1.151-185.2001},  Journal = {Microbiol Mol Biol Rev},  Journal-Full = {Microbiology and molecular biology reviews : MMBR},  Mesh = {Evolution; Genes, Viral; HIV; Humans; Markov Chains; Mathematics; Models, Biological; Polymorphism, Genetic; Selection Bias; Selection, Genetic; Stochastic Processes; Viruses},  Month = {Mar},  Number = {1},  Pages = {151-85},  Pmc = {PMC99023},  Pmid = {11238990},  Pst = {ppublish},  Title = {Transition between stochastic evolution and deterministic evolution in the presence of selection: general theory and application to virology},  Volume = {65},  Year = {2001},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/MMBR.65.1.151-185.2001}}  @article{Rouzine:2007ly,  Abstract = {Earlier, using the semi-deterministic solitary wave approach, we have investigated accumulation of pre-existing beneficial alleles in genomes consisting of a large number of simultaneously evolving sites in the presence of selection and infrequent recombination with small rate r per genome. Our previous results for the dynamics of the fitness distribution of genomes are now interpreted in terms of the life cycle of recombinant clones. We show that, at sufficiently small r, the clones dominating fitness classes, at the moment of their birth, are nearly the best fit in a population. New progeny clones are mostly generated by parental genomes whose fitness falls within a narrow interval in the middle of the high-fitness tail of fitness distribution. We also derive the fitness distribution for the distant ancestors of sites of a randomly sampled genome and show that its form is controlled by a single composite model parameter proportional to r. The ancestral fitness distribution differs dramatically from the fitness distribution of the entire ancient population: it is much broader and localized in the high-fitness tail of the ancient population. We generalize these results to the case of moderately small r to conclude that, regardless of fitness of an individual, all its distant ancestors are exceptionally well fit.},  Author = {Rouzine, I M and Coffin, J M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.tpb.2006.09.002},  Journal = {Theor Popul Biol},  Journal-Full = {Theoretical population biology},  Mesh = {Family; Genetic Determinism; Genetics, Population; Genome; Haploidy; Humans; Linkage (Genetics); Models, Genetic; Pedigree; Population Dynamics; Recombination, Genetic; Selection, Genetic},  Month = {Mar},  Number = {2},  Pages = {239-50},  Pmc = {PMC1994660},  Pmid = {17097121},  Pst = {ppublish},  Title = {Highly fit ancestors of a partly sexual haploid population},  Volume = {71},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tpb.2006.09.002}}  @article{saitou:1987ne,  Author = {Saitou, N and Nei, M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Molecular Biology and Evolution},  Month = jul,  Number = {4},  Pages = {406--425},  Title = {The neighbor-joining method: a new method for reconstructing phylogenetic trees},  Url = {http://mbe.oxfordjournals.org/cgi/content/abstract/4/4/406},  Volume = {4},  Year = {1987},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/4/4/406}}  @article{salemi:2000da,  Abstract = {Attempts to estimate the time of origin of human immunodeficiency virus {(HIV)-1} by using phylogenetic analysis are seriously flawed because of the unequal evolutionary rates among different viral lineages. Here, we report a new method of molecular clock analysis, called Site Stripping for Clock Detection {(SSCD),} which allows selection of nucleotide sites evolving at an equal rate in different lineages. The method was validated on a dataset of patients all infected with hepatitis C virus in 1977 by the same donor, and it was able to date exactly the �known� origin of the infection. Using the same method, we calculated that the origin of {HIV-1} group M radiation was in the 1930s. In addition, we show that the coalescence time of the simian ancestor of {HIV-1} group M and its closest related cpz strains occurred around the end of the {XVII} century, a date that could be considered the upper limit to the time of simian-to-human transmission of {HIV-1} group M. The results show also that {SSCD} is an easy-to-use method of general applicability in molecular evolution to calibrate clock-like phylogenetic trees. Key words: interspecies transmission � molecular clock},  Author = {Salemi, Marco and Strimmer, Korbinian and Hall, William W. and Duffy, Margaret and Delaporte, Eric and Mboup, Souleymane and Peeters, Martine and Vandamme, {Anne-Mieke}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1096/fj.00-0449fje},  Journal = {{FASEB} J.},  Month = dec,  Pages = {00--0449fje},  Title = {Dating the common ancestor of {SIVcpz} and {HIV-1} group M and the origin of {HIV-1} subtypes by using a new method to uncover clock-like molecular evolution},  Url = {http://www.fasebj.org/cgi/content/abstract/00-0449fjev1},  Year = {2000},  Bdsk-Url-1 = {http://www.fasebj.org/cgi/content/abstract/00-0449fjev1},  Bdsk-Url-2 = {http://dx.doi.org/10.1096/fj.00-0449fje}}  @article{salemi:2008hi,  Abstract = {Background

HIV-1 epidemic in Western Europe is largely due to subtype B. Little is known about the HIV-1 in Eastern Europe, but a few studies have shown that non-B subtypes are quite common. In Albania, where a recent study estimated a ten-fold increase of AIDS incidence during the last six years, subtype A and B account for 90\% of the know infections.

Methodology/Principal Findings

We investigated the demographic history of HIV-1 subtype A and B in Albania by using a statistical framework based on coalescent theory and phylogeography. High-resolution phylogenetic and molecular clock analysis showed a limited introduction to the Balkan country of subtype A during the late 1980s followed by an epidemic outburst in the early 1990s. In contrast, subtype B was apparently introduced multiple times between the mid-1970s and mid-1980s. Both subtypes are growing exponentially, although the HIV-1A epidemic displays a faster growth rate, and a significantly higher basic reproductive number R0. HIV-1A gene flow occurs primarily from the capital Tirane, in the center of the country, to the periphery, while HIV-1B flow is characterized by a balanced exchange between center and periphery. Finally, we calculated that the actual number of infections in Albania is at least two orders of magnitude higher than previously thought.

Conclusions/Significance

Our analysis demonstrates the power of recently developed computational tools to investigate molecular epidemiology of pathogens, and emphasize the complex factors involved in the establishment of HIV-1 epidemics. We suggest that a significant correlation exists between HIV-1 exponential spread and the socio-political changes occurred during the Balkan wars. The fast growth of a relatively new non-B epidemic in the Balkans may have significant consequences for the evolution of HIV-1 epidemiology in neighboring countries in Eastern and Western Europe.

},
  Author = {Salemi, Marco and de Oliveira, Tulio and Ciccozzi, Massimo and Rezza, Giovanni and Goodenow, Maureen M.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pone.0001390},  Journal = {PLoS ONE},  Month = {01},  Number = {1},  Pages = {e1390},  Publisher = {Public Library of Science},  Title = {High-Resolution Molecular Epidemiology and Evolutionary History of HIV-1 Subtypes in Albania},  Url = {http://dx.plos.org/10.1371%2Fjournal.pone.0001390},  Volume = {3},  Year = {2008},  Bdsk-Url-1 = {http://dx.plos.org/10.1371/journal.pone.0001390},  Bdsk-Url-2 = {http://dx.doi.org/10.1371/journal.pone.0001390}}  @article{salminen:1995:id,  Annote = {{PMID:} 8573403},  Author = {Salminen, M.O. and Carr, J.K. and Burke, D.S. and McCutchan, F.E.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {{AIDS} Research and Human Retroviruses},  Number = {11},  Pages = {1423--1425},  Title = {Identification of Breakpoints in Intergenotypic Recombinants of {HIV} Type 1 by Bootscanning},  Url = {http://dx.doi.org/10.1089/aid.1995.11.1423},  Volume = {11},  Year = {1995},  Bdsk-Url-1 = {http://dx.doi.org/10.1089/aid.1995.11.1423}}  @article{sanderson:1997no,  Author = {Sanderson, {MJ}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Molecular Biology and Evolution},  Month = dec,  Number = {12},  Pages = {1218--1231},  Title = {A Nonparametric Approach to Estimating Divergence Times in the Absence of Rate Constancy},  Url = {http://mbe.oxfordjournals.org.ezproxy.auckland.ac.nz/cgi/reprint/14/12/1218},  Volume = {14},  Year = {1997},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org.ezproxy.auckland.ac.nz/cgi/reprint/14/12/1218}}  @article{sanderson:2002es,  Abstract = {Rates of molecular evolution vary widely between lineages, but quantification of how rates change has proven difficult. Recently proposed estimation procedures have mainly adopted highly parametric approaches that model rate evolution explicitly. In this study, a semiparametric smoothing method is developed using penalized likelihood. A saturated model in which every lineage has a separate rate is combined with a roughness penalty that discourages rates from varying too much across a phylogeny. A data-driven cross-validation criterion is then used to determine an optimal level of smoothing. This criterion is based on an estimate of the average prediction error associated with pruning lineages from the tree. The methods are applied to three data sets of six genes across a sample of land plants. Optimally smoothed estimates of absolute rates entailed 2- to 10-fold variation across lineages.},  Author = {Sanderson, Michael J.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Molecular Biology and Evolution},  Month = jan,  Number = {1},  Pages = {101--109},  Title = {Estimating Absolute Rates of Molecular Evolution and Divergence Times: A Penalized Likelihood Approach},  Url = {http://mbe.oxfordjournals.org/cgi/content/abstract/19/1/101},  Volume = {19},  Year = {2002},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/19/1/101}}  @article{sanmartin:2008in,  Abstract = {Aim Oceanic islands represent a special challenge to historical biogeographers because dispersal is typically the dominant process while most existing methods are based on vicariance. Here, we describe a new Bayesian approach to island biogeography that estimates island carrying capacities and dispersal rates based on simple Markov models of biogeographical processes. This is done in the context of simultaneous analysis of phylogenetic and distributional data across groups, accommodating phylogenetic uncertainty and making parameter estimates more robust. We test our models on an empirical data set of published phylogenies of Canary Island organisms to examine overall dispersal rates and correlation of rates with explanatory factors such as geographic proximity and area {size.Location} Oceanic archipelagos with special reference to the Atlantic Canary {Islands.Methods} The Canary Islands were divided into three island-groups, corresponding to the main magmatism periods in the formation of the archipelago, while {non-Canarian} distributions were grouped into a fourth 'mainland-island'. Dispersal between island groups, which were assumed constant through time, was modelled as a homogeneous, time-reversible Markov process, analogous to the standard models of {DNA} evolution. The stationary state frequencies in these models reflect the relative carrying capacity of the islands, while the exchangeability (rate) parameters reflect the relative dispersal rates between islands. We examined models of increasing complexity: {Jukes2013Cantor} {(JC),} Equal-in, and General Time Reversible {(GTR),} with or without the assumption of stepping-stone dispersal. The data consisted of 13 Canarian phylogenies: 954 individuals representing 393 taxonomic (morphological) entities. Each group was allowed to evolve under its own {DNA} model, with the island-model shared across groups. Posterior distributions on island model parameters were estimated using Markov Chain Monte Carlo {(MCMC)} sampling, as implemented in {MrBayes} 4.0, and Bayes Factors were used to compare {models.Results} The Equal-in step, the {GTR,} and the {GTR} step dispersal models showed the best fit to the data. In the Equal-in and {GTR} models, the largest carrying capacity was estimated for the mainland, followed by the central islands and the western islands, with the eastern islands having the smallest carrying capacity. The relative dispersal rate was highest between the central and eastern islands, and between the central and western islands. The exchange with the mainland was rare in {comparison.Main} conclusions Our results confirm those of earlier studies suggesting that inter-island dispersal within the Canary Island archipelago has been more important in explaining diversification within lineages than dispersal between the continent and the islands, despite the close proximity to North Africa. The low carrying capacity of the eastern islands, uncorrelated with their size or age, fits well with the idea of a historically depauperate biota in these islands but more sophisticated models are needed to address the possible influence of major recent extinction events. The island models explored here can easily be extended to address other problems in historical biogeography, such as dispersal among areas in continental settings or reticulate area relationships.},  Author = {Sanmart{\'\i}n, Isabel and van der Mark, Paul and Ronquist, Fredrik},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1111/j.1365-2699.2008.01885.x},  Journal = {Journal of Biogeography},  Number = {3},  Pages = {428--449},  Shorttitle = {Inferring dispersal},  Title = {Inferring dispersal: a Bayesian approach to phylogeny-based island biogeography, with special reference to the Canary Islands},  Url = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1111/j.1365-2699.2008.01885.x},  Volume = {35},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1111/j.1365-2699.2008.01885.x},  Bdsk-Url-2 = {http://dx.doi.org/10.1111/j.1365-2699.2008.01885.x}}  @article{santiago:2002si,  Author = {Santiago, Mario L. and Rodenburg, Cynthia M. and Kamenya, Shadrack and {Bibollet-Ruche}, Frederic and Gao, Feng and Bailes, Elizabeth and Meleth, Sreelatha and Soong, {Seng-Jaw} and Kilby, J. Michael and Moldoveanu, Zina and Fahey, Babette and Muller, Martin N. and Ayouba, Ahidjo and Nerrienet, Eric and {McClure}, Harold M. and Heeney, Jonathan L. and Pusey, Anne E. and Collins, D. Anthony and Boesch, Christophe and Wrangham, Richard W. and Goodall, Jane and Sharp, Paul M. and Shaw, George M. and Hahn, Beatrice H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.295.5554.465},  Journal = {Science},  Month = jan,  Number = {5554},  Pages = {465},  Title = {{SIVcpz} in Wild Chimpanzees},  Url = {http://www.sciencemag.org},  Volume = {295},  Year = {2002},  Bdsk-Url-1 = {http://www.sciencemag.org},  Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.295.5554.465}}  @article{santiago:2005si,  Abstract = {Simian immunodeficiency virus of sooty mangabeys {(SIVsmm)} is recognized as the progenitor of human immunodeficiency virus type 2 {(HIV-2)} and has been transmitted to humans on multiple occasions, yet the epidemiology and genetic diversity of {SIVsmm} infection in wild-living populations remain largely unknown. Here, we report the first molecular epidemiological survey of {SIVsmm} in a community of [{\textasciitilde}]120 free-ranging sooty mangabeys in the Tai Forest, Cote {d'Ivoire.} Fecal samples (n = 39) were collected from 35 habituated animals (27 females and 8 males) and tested for {SIVsmm} virion {RNA} {(vRNA).} Viral gag (800 bp) and/or env (490 bp) sequences were amplified from 11 different individuals (eight females and three males). Based on the sensitivity of fecal {vRNA} detection and the numbers of samples analyzed, the prevalence of {SIVsmm} infection was estimated to be 59\% (95\% confidence interval, 0.35 to 0.88). Behavioral data collected from this community indicated that {SIVsmm} infection occurred preferentially in high-ranking females. Phylogenetic analysis of gag and env sequences revealed an extraordinary degree of genetic diversity, including evidence for frequent recombination events in both the recent and distant past. Some sooty mangabeys harbored near-identical viruses ({\textless}2\% interstrain distance), indicating epidemiologically linked infections. These transmissions were identified by microsatellite analyses to involve both related (mother/daughter) and unrelated individuals, thus providing evidence for vertical and horizontal transmission in the wild. Finally, evolutionary tree analyses revealed significant clustering of the Tai {SIVsmm} strains with five of the eight recognized groups of {HIV-2,} including the epidemic groups A and B, thus pointing to a likely geographic origin of these human infections in the eastern part of the sooty mangabey range.},  Author = {Santiago, Mario L. and Range, Friederike and Keele, Brandon F. and Li, Yingying and Bailes, Elizabeth and {Bibollet-Ruche}, Frederic and Fruteau, Cecile and Noe, Ronald and Peeters, Martine and Brookfield, John F. Y. and Shaw, George M. and Sharp, Paul M. and Hahn, Beatrice H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.79.19.12515-12527.2005},  Journal = {The Journal of Virology},  Month = oct,  Number = {19},  Pages = {12515--12527},  Title = {Simian Immunodeficiency Virus Infection in {Free-Ranging} Sooty Mangabeys {(Cercocebus} atys atys) from the Tai Forest, Cote {d'Ivoire:} Implications for the Origin of Epidemic Human Immunodeficiency Virus Type 2},  Url = {http://jvi.asm.org/cgi/content/abstract/79/19/12515},  Volume = {79},  Year = {2005},  Bdsk-Url-1 = {http://jvi.asm.org/cgi/content/abstract/79/19/12515},  Bdsk-Url-2 = {http://dx.doi.org/10.1128/JVI.79.19.12515-12527.2005}}  @article{schwartz:2010br,  Abstract = {{BACKGROUND:Estimates} of divergence dates between species improve our understanding of processes ranging from nucleotide substitution to speciation. Such estimates are frequently based on molecular genetic differences between species; therefore, they rely on accurate estimates of the number of such differences (i.e. substitutions per site, measured as branch length on phylogenies). We used simulations to determine the effects of dataset size, branch length heterogeneity, branch depth, and analytical framework on branch length estimation across a range of branch lengths. We then reanalyzed an empirical dataset for plethodontid salamanders to determine how inaccurate branch length estimation can affect estimates of divergence {dates.RESULTS:The} accuracy of branch length estimation varied with branch length, dataset size (both number of taxa and sites), branch length heterogeneity, branch depth, dataset complexity, and analytical framework. For simple phylogenies analyzed in a Bayesian framework, branches were increasingly underestimated as branch length increased; in a maximum likelihood framework, longer branch lengths were somewhat overestimated. Longer datasets improved estimates in both frameworks; however, when the number of taxa was increased, estimation accuracy for deeper branches was less than for tip branches. Increasing the complexity of the dataset produced more misestimated branches in a Bayesian framework; however, in an {ML} framework, more branches were estimated more accurately. Using {ML} branch length estimates to re-estimate plethodontid salamander divergence dates generally resulted in an increase in the estimated age of older nodes and a decrease in the estimated age of younger {nodes.CONCLUSIONS:Branch} lengths are misestimated in both statistical frameworks for simulations of simple datasets. However, for complex datasets, length estimates are quite accurate in {ML} (even for short datasets), whereas few branches are estimated accurately in a Bayesian framework. Our reanalysis of empirical data demonstrates the magnitude of effects of Bayesian branch length misestimation on divergence date estimates. Because the length of branches for empirical datasets can be estimated most reliably in an {ML} framework when branches are {\textless}1 substitution/site and datasets are [greater than or equal to]1 kb, we suggest that divergence date estimates using datasets, branch lengths, and/or analytical techniques that fall outside of these parameters should be interpreted with caution.},  Author = {Schwartz, Rachel and Mueller, Rachel},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {{BMC} Evolutionary Biology},  Number = {1},  Pages = {5},  Title = {Branch length estimation and divergence dating: estimates of error in Bayesian and maximum likelihood frameworks},  Url = {http://www.biomedcentral.com/1471-2148/10/5},  Volume = {10},  Year = {2010},  Bdsk-Url-1 = {http://www.biomedcentral.com/1471-2148/10/5}}  @article{seo:2002vi,  Abstract = {Motivation: The high pace of viral sequence change means that  variation in the times at which sequences are sampled can have a  profound effect both on the ability to detect trends over time in  evolutionary rates and on the power to reject the Molecular Clock  Hypothesis {(MCH).} Trends in viral evolutionary rates are of  particular interest because their detection may allow connections to  be established between a patient's treatment or condition and  the process of evolution. Variation in sequence isolation times also  impacts the uncertainty associated with estimates of divergence  times and evolutionary rates. Variation in isolation times can be  intentionally adjusted to increase the power of hypothesis tests and  to reduce the uncertainty of evolutionary parameter estimates, but  this fact has received little previous {attention.Results:} We provide approximations for the power to reject the  {MCH} when the alternative is that rates change in a linear fashion  over time and when the alternative is that rates differ randomly  among branches. In addition, we approximate the standard deviation  of estimated evolutionary rates and divergence times. We illustrate  how these approximations can be exploited to determine which viral  sample to sequence when samples representing different dates are  {available.Contact:} [email protected]; [email protected];  [email protected];  [email protected]},  Author = {Seo, Tae-{K}un and Thorne, Jeffrey L. and Hasegawa, Masami and Kishino, Hirohisa},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 03:45:03 +0000},  Doi = {10.1093/bioinformatics/18.1.115},  Journal = {Bioinformatics},  Month = jan,  Number = {1},  Pages = {115 --123},  Title = {A viral sampling design for testing the molecular clock and for estimating evolutionary rates and divergence times},  Volume = {18},  Year = {2002},  Bdsk-Url-1 = {http://bioinformatics.oxfordjournals.org/content/18/1/115.abstract},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/bioinformatics/18.1.115}}  @article{shapiro:2010ba,  Author = {Shapiro, B. and Ho, S. Y. W. and Drummond, A. J. and Suchard, M. A. and Pybus, O. G. and Rambaut, A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 00:55:00 +0000},  Issn = {0737-4038},  Journal = {Molecular Biology and Evolution},  Publisher = {SMBE},  Title = {{A Bayesian phylogenetic method to estimate unknown sequence ages}},  Year = {2010}}  @article{sharp:2000or,  Author = {Sharp, P. and Bailes, E. and Gao, F. and Beer, B. and Hirsch, V. and Hahn, B.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Biochemical society transactions},  Number = {part 2},  Pages = {275--282},  Title = {{Origins and evolution of AIDS viruses: estimating the time-scale}},  Volume = {28},  Year = {2000}}  @article{sharp:2001or,  Abstract = {In the absence of direct epidemiological evidence, molecular evolutionary studies of primate lentiviruses provide the most definitive information about the origins of human immunodeficiency virus {(HIV)--1} and {HIV--2.} Related lentiviruses have been found infecting numerous species of primates in {sub--Saharan} Africa. The only species naturally infected with viruses closely related to {HIV--2} is the sooty mangabey {(Cercocebus} atys) from western Africa, the region where {HIV--2} is known to be endemic. Similarly, the only viruses very closely related to {HIV--1} have been isolated from chimpanzees {(Pan} troglodytes), and in particular those from western equatorial Africa, again coinciding with the region that appears to be the hearth of the {HIV--1} pandemic. {HIV--1} and {HIV--2} have each arisen several times: in the case of {HIV--1,} the three groups {(M,} N and O) are the result of independent cross--species transmission events. Consistent with the phylogenetic position of a `fossil' virus from 1959, molecular clock analyses using realistic models of {HIV--1} sequence evolution place the last common ancestor of the M group prior to 1940, and several lines of evidence indicate that the jump from chimpanzees to humans occurred before then. Both the inferred geographical origin of {HIV--1} and the timing of the cross--species transmission are inconsistent with the suggestion that oral polio vaccines, putatively contaminated with viruses from chimpanzees in eastern equatorial Africa in the late 1950s, could be responsible for the origin of acquired immune deficiency syndrome.},  Author = {Sharp, Paul M. and Bailes, Elizabeth and Chaudhuri, Roy R. and Rodenburg, Cynthia M. and Santiago, Mario O. and Hahn, Beatrice H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1098/rstb.2001.0863},  Journal = {Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences},  Month = jun,  Number = {1410},  Pages = {867 --876},  Title = {The origins of acquired immune deficiency syndrome viruses: where and when?},  Url = {http://rstb.royalsocietypublishing.org/content/356/1410/867.abstract},  Volume = {356},  Year = {2001},  Bdsk-Url-1 = {http://rstb.royalsocietypublishing.org/content/356/1410/867.abstract},  Bdsk-Url-2 = {http://dx.doi.org/10.1098/rstb.2001.0863}}  @article{sharp:2010ev,  Abstract = {The major cause of acquired immune deficiency syndrome {(AIDS)} is human immunodeficiency virus type 1 {(HIV-1).} We have been using evolutionary comparisons to trace (i) the origin(s) of {HIV-1} and (ii) the origin(s) of {AIDS.} The closest relatives of {HIV-1} are simian immunodeficiency viruses {(SIVs)} infecting wild-living chimpanzees {(Pan} troglodytes troglodytes) and gorillas {(Gorilla} gorilla gorilla) in west central Africa. Phylogenetic analyses have revealed the origins of {HIV-1:} chimpanzees were the original hosts of this clade of viruses; four lineages of {HIV-1} have arisen by independent cross-species transmissions to humans and one or two of those transmissions may have been via gorillas. However, {SIVs} are primarily monkey viruses: more than 40 species of African monkeys are infected with their own, species-specific, {SIV} and in at least some host species, the infection seems non-pathogenic. Chimpanzees acquired from monkeys two distinct forms of {SIVs} that recombined to produce a virus with a unique genome structure. We have found that {SIV} infection causes {CD4+} T-cell depletion and increases mortality in wild chimpanzees, and so the origin of {AIDS} is more ancient than the origin of {HIV-1.} Tracing the genetic changes that occurred as monkey viruses adapted to infect first chimpanzees and then humans may provide insights into the causes of the pathogenicity of these viruses.},  Author = {Sharp, Paul M. and Hahn, Beatrice H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1098/rstb.2010.0031},  Journal = {Philosophical Transactions of the Royal Society B: Biological Sciences},  Number = {1552},  Pages = {2487 --2494},  Title = {The evolution of {HIV-1} and the origin of {AIDS}},  Url = {http://rstb.royalsocietypublishing.org/content/365/1552/2487.abstract},  Volume = {365},  Year = {2010},  Bdsk-Url-1 = {http://rstb.royalsocietypublishing.org/content/365/1552/2487.abstract},  Bdsk-Url-2 = {http://dx.doi.org/10.1098/rstb.2010.0031}}  @article{Siebenga:2010fk,  Abstract = {Noroviruses are the most common cause of viral gastroenteritis. An increase in the number of globally reported norovirus outbreaks was seen the past decade, especially for outbreaks caused by successive genogroup II genotype 4 (GII.4) variants. Whether this observed increase was due to an upswing in the number of infections, or to a surveillance artifact caused by heightened awareness and concomitant improved reporting, remained unclear. Therefore, we set out to study the population structure and changes thereof of GII.4 strains detected through systematic outbreak surveillance since the early 1990s. We collected 1383 partial polymerase and 194 full capsid GII.4 sequences. A Bayesian MCMC coalescent analysis revealed an increase in the number of GII.4 infections during the last decade. The GII.4 strains included in our analyses evolved at a rate of 4.3-9.0x10(-3) mutations per site per year, and share a most recent common ancestor in the early 1980s. Determinants of adaptation in the capsid protein were studied using different maximum likelihood approaches to identify sites subject to diversifying or directional selection and sites that co-evolved. While a number of the computationally determined adaptively evolving sites were on the surface of the capsid and possible subject to immune selection, we also detected sites that were subject to constrained or compensatory evolution due to secondary RNA structures, relevant in virus-replication. We highlight codons that may prove useful in identifying emerging novel variants, and, using these, indicate that the novel 2008 variant is more likely to cause a future epidemic than the 2007 variant. While norovirus infections are generally mild and self-limiting, more severe outcomes of infection frequently occur in elderly and immunocompromized people, and no treatment is available. The observed pattern of continually emerging novel variants of GII.4, causing elevated numbers of infections, is therefore a cause for concern.},  Author = {Siebenga, J Joukje and Lemey, Philippe and Kosakovsky Pond, Sergei L and Rambaut, Andrew and Vennema, Harry and Koopmans, Marion},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.ppat.1000884},  Journal = {PLoS Pathog},  Journal-Full = {PLoS pathogens},  Mesh = {Amino Acid Substitution; Bayes Theorem; Caliciviridae Infections; Capsid Proteins; Dimerization; Disease Outbreaks; Epistasis, Genetic; Evolution, Molecular; Gastroenteritis; Models, Genetic; Norovirus; Nucleic Acid Conformation; Open Reading Frames; Phylogeny; RNA, Viral; Virus Replication},  Month = {May},  Number = {5},  Pages = {e1000884},  Pmc = {PMC2865530},  Pmid = {20463813},  Pst = {epublish},  Title = {Phylodynamic reconstruction reveals norovirus GII.4 epidemic expansions and their molecular determinants},  Volume = {6},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.ppat.1000884}}  @article{simmonds:2001or,  Author = {Simmonds, P.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {The Journal of general virology},  Number = {Pt 4},  Pages = {693},  Title = {{The origin and evolution of hepatitis viruses in humans.}},  Volume = {82},  Year = {2001}}  @article{slatkin:1989cl,  Author = {Slatkin, M. and Maddison, W. P.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-27 15:57:41 +1300},  Journal = {Genetics},  Month = nov,  Number = {3},  Pages = {603--613},  Title = {A Cladistic Measure of Gene Flow Inferred from the Phylogenies of Alleles},  Volume = {123},  Year = {1989},  Bdsk-Url-1 = {http://www.genetics.org/cgi/content/abstract/123/3/603}}  @article{smith:1992:an,  Author = {Smith, {JohnMaynard}},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1007/BF00182389},  Issn = {0022-2844},  Journal = {Journal of Molecular Evolution},  Number = {2},  Title = {Analyzing the mosaic structure of genes},  Url = {http://www.springerlink.com.ezproxy.auckland.ac.nz/content/n185628502116551/},  Volume = {34},  Year = {1992},  Bdsk-Url-1 = {http://www.springerlink.com.ezproxy.auckland.ac.nz/content/n185628502116551/},  Bdsk-Url-2 = {http://dx.doi.org/10.1007/BF00182389}}  @article{Smith:2009fv,  Abstract = {In March and early April 2009, a new swine-origin influenza A (H1N1) virus (S-OIV) emerged in Mexico and the United States. During the first few weeks of surveillance, the virus spread worldwide to 30 countries (as of May 11) by human-to-human transmission, causing the World Health Organization to raise its pandemic alert to level 5 of 6. This virus has the potential to develop into the first influenza pandemic of the twenty-first century. Here we use evolutionary analysis to estimate the timescale of the origins and the early development of the S-OIV epidemic. We show that it was derived from several viruses circulating in swine, and that the initial transmission to humans occurred several months before recognition of the outbreak. A phylogenetic estimate of the gaps in genetic surveillance indicates a long period of unsampled ancestry before the S-OIV outbreak, suggesting that the reassortment of swine lineages may have occurred years before emergence in humans, and that the multiple genetic ancestry of S-OIV is not indicative of an artificial origin. Furthermore, the unsampled history of the epidemic means that the nature and location of the genetically closest swine viruses reveal little about the immediate origin of the epidemic, despite the fact that we included a panel of closely related and previously unpublished swine influenza isolates. Our results highlight the need for systematic surveillance of influenza in swine, and provide evidence that the mixing of new genetic elements in swine can result in the emergence of viruses with pandemic potential in humans.},  Author = {Smith, Gavin J D and Vijaykrishna, Dhanasekaran and Bahl, Justin and Lycett, Samantha J and Worobey, Michael and Pybus, Oliver G and Ma, Siu Kit and Cheung, Chung Lam and Raghwani, Jayna and Bhatt, Samir and Peiris, J S Malik and Guan, Yi and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nature08182},  Journal = {Nature},  Journal-Full = {Nature},  Mesh = {Animals; Disease Outbreaks; Evolution, Molecular; Genome, Viral; Humans; Influenza A Virus, H1N1 Subtype; Influenza, Human; Molecular Sequence Data; Orthomyxoviridae Infections; Phylogeny; Reassortant Viruses; Swine; Swine Diseases; Time Factors},  Month = {Jun},  Number = {7250},  Pages = {1122-5},  Pmid = {19516283},  Pst = {ppublish},  Title = {Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic},  Volume = {459},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature08182}}  @article{Smith:2009ss,  Abstract = {Pandemic influenza viruses cause significant mortality in humans. In the 20th century, 3 influenza viruses caused major pandemics: the 1918 H1N1 virus, the 1957 H2N2 virus, and the 1968 H3N2 virus. These pandemics were initiated by the introduction and successful adaptation of a novel hemagglutinin subtype to humans from an animal source, resulting in antigenic shift. Despite global concern regarding a new pandemic influenza, the emergence pathway of pandemic strains remains unknown. Here we estimated the evolutionary history and inferred date of introduction to humans of each of the genes for all 20th century pandemic influenza strains. Our results indicate that genetic components of the 1918 H1N1 pandemic virus circulated in mammalian hosts, i.e., swine and humans, as early as 1911 and was not likely to be a recently introduced avian virus. Phylogenetic relationships suggest that the A/Brevig Mission/1/1918 virus (BM/1918) was generated by reassortment between mammalian viruses and a previously circulating human strain, either in swine or, possibly, in humans. Furthermore, seasonal and classic swine H1N1 viruses were not derived directly from BM/1918, but their precursors co-circulated during the pandemic. Mean estimates of the time of most recent common ancestor also suggest that the H2N2 and H3N2 pandemic strains may have been generated through reassortment events in unknown mammalian hosts and involved multiple avian viruses preceding pandemic recognition. The possible generation of pandemic strains through a series of reassortment events in mammals over a period of years before pandemic recognition suggests that appropriate surveillance strategies for detection of precursor viruses may abort future pandemics.},  Author = {Smith, Gavin J D and Bahl, Justin and Vijaykrishna, Dhanasekaran and Zhang, Jinxia and Poon, Leo L M and Chen, Honglin and Webster, Robert G and Peiris, J S Malik and Guan, Yi},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1073/pnas.0904991106},  Journal = {Proc Natl Acad Sci U S A},  Journal-Full = {Proceedings of the National Academy of Sciences of the United States of America},  Mesh = {Bayes Theorem; Cluster Analysis; Disease Outbreaks; Evolution, Molecular; History, 20th Century; Humans; Influenza A virus; Influenza, Human; Models, Genetic; Phylogeny},  Month = {Jul},  Number = {28},  Pages = {11709-12},  Pmc = {PMC2709671},  Pmid = {19597152},  Pst = {ppublish},  Title = {Dating the emergence of pandemic influenza viruses},  Volume = {106},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0904991106}}  @article{sneath:1973:nu,  Author = {Sneath, P.H.A. and Sokal, R.R.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {San Francisco},  Title = {{Numerical taxonomy: the principles and practice of numerical classification}},  Volume = {21},  Year = {1973}}  @article{Stack:2010fk,  Abstract = {With more emphasis being put on global infectious disease monitoring, viral genetic data are being collected at an astounding rate, both within and without the context of a long-term disease surveillance plan. Concurrent with this increase have come improvements to the sophisticated and generalized statistical techniques used for extracting population-level information from genetic sequence data. However, little research has been done on how the collection of these viral sequence data can or does affect the efficacy of the phylogenetic algorithms used to analyse and interpret them. In this study, we use epidemic simulations to consider how the collection of viral sequence data clarifies or distorts the picture, provided by the phylogenetic algorithms, of the underlying population dynamics of the simulated viral infection over many epidemic cycles. We find that sampling protocols purposefully designed to capture sequences at specific points in the epidemic cycle, such as is done for seasonal influenza surveillance, lead to a significantly better view of the underlying population dynamics than do less-focused collection protocols. Our results suggest that the temporal distribution of samples can have a significant effect on what can be inferred from genetic data, and thus highlight the importance of considering this distribution when designing or evaluating protocols and analysing the data collected thereunder.},  Author = {Stack, J Conrad and Welch, J David and Ferrari, Matt J and Shapiro, Beth U and Grenfell, Bryan T},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1098/rsif.2009.0530},  Journal = {J R Soc Interface},  Journal-Full = {Journal of the Royal Society, Interface / the Royal Society},  Mesh = {Base Sequence; Disease Outbreaks; Humans; Influenza, Human; Population Dynamics},  Month = {Jul},  Number = {48},  Pages = {1119-27},  Pmc = {PMC2880085},  Pmid = {20147314},  Pst = {ppublish},  Title = {Protocols for sampling viral sequences to study epidemic dynamics},  Volume = {7},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rsif.2009.0530}}  @article{Stadler:2009fk,  Abstract = {The constant rate birth-death process is used as a stochastic model for many biological systems, for example phylogenies or disease transmission. As the biological data are usually not fully available, it is crucial to understand the effect of incomplete sampling. In this paper, we analyze the constant rate birth-death process with incomplete sampling. We derive the density of the bifurcation events for trees on n leaves which evolved under this birth-death-sampling process. This density is used for calculating prior distributions in Bayesian inference programs and for efficiently simulating trees. We show that the birth-death-sampling process can be interpreted as a birth-death process with reduced rates and complete sampling. This shows that joint inference of birth rate, death rate and sampling probability is not possible. The birth-death-sampling process is compared to the sampling-based population genetics model, the coalescent. It is shown that despite many similarities between these two models, the distribution of bifurcation times remains different even in the case of very large population sizes. We illustrate these findings on an Hepatitis C virus dataset from Egypt. We show that the transmission times estimates are significantly different-the widely used Gamma statistic even changes its sign from negative to positive when switching from the coalescent to the birth-death process.},  Author = {Stadler, Tanja},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:58:49 +0000},  Doi = {10.1016/j.jtbi.2009.07.018},  Journal = {J Theor Biol},  Journal-Full = {Journal of theoretical biology},  Mesh = {Animals; Birth Rate; Egypt; Hepatitis C; Humans; Models, Biological; Phylogeny; Population Density; Population Dynamics; Stochastic Processes},  Month = {11},  Number = {1},  Pages = {58-66},  Pmid = {19631666},  Pst = {ppublish},  Title = {On incomplete sampling under birth-death models and connections to the sampling-based coalescent},  Volume = {261},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jtbi.2009.07.018}}  @article{Stadler:2010kx,  Abstract = {I consider the constant rate birth-death process with incomplete sampling. I calculate the density of a given tree with sampled extant and extinct individuals. This density is essential for analyzing datasets which are sampled through time. Such datasets are common in virus epidemiology as viruses in infected individuals are sampled through time. Further, such datasets appear in phylogenetics when extant and extinct species data is available. I show how the derived tree density can be used (i) as a tree prior in a Bayesian method to reconstruct the evolutionary past of the sequence data on a calender-timescale, (ii) to infer the birth- and death-rates for a reconstructed evolutionary tree, and (iii) for simulating trees with a given number of sampled extant and extinct individuals which is essential for testing evolutionary hypotheses for the considered datasets.},  Author = {Stadler, Tanja},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:59:03 +0000},  Doi = {10.1016/j.jtbi.2010.09.010},  Journal = {J Theor Biol},  Journal-Full = {Journal of theoretical biology},  Month = {12},  Number = {3},  Pages = {396-404},  Pmid = {20851708},  Pst = {ppublish},  Title = {Sampling-through-time in birth-death trees},  Volume = {267},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.jtbi.2010.09.010}}  @article{stanhope:2004ev,  Annote = {The origins and evolutionary history of the Severe Acute Respiratory Syndrome {(SARS)} coronavirus {(SARS-CoV)} remain an issue of uncertainty and debate. Based on evolutionary analyses of coronavirus {DNA} sequences, encompassing an approximately 13�kb stretch of the {SARS-TOR2} genome, we provide evidence that {SARS-CoV} has a recombinant history with lineages of types I and {III} coronavirus. We identified a minimum of five recombinant regions ranging from 83 to 863�bp in length and including the polymerase, nsp9, nsp10, and nsp14. Our results are consistent with a hypothesis of viral host jumping events, concomitant with the reassortment of bird and mammalian coronaviruses, a scenario analogous to earlier outbreaks of influenzae.},  Author = {Stanhope, Michael J. and Brown, James R. and {Amrine-Madsen}, Heather},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1016/j.meegid.2003.10.001},  Issn = {1567-1348},  Journal = {Infection, Genetics and Evolution},  Keywords = {Coronavirus, Phylogeny, recombination, Severe acute respiratory syndrome, Viral host-shift},  Number = {1},  Pages = {15--19},  Title = {Evidence from the evolutionary analysis of nucleotide sequences for a recombinant history of {SARS-CoV}},  Url = {http://www.sciencedirect.com/science/article/B6W8B-4B7Y1FV-1/2/8b3c7f9095b6b149f8886c3a1d8c69c8},  Volume = {4},  Year = {2004},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6W8B-4B7Y1FV-1/2/8b3c7f9095b6b149f8886c3a1d8c69c8},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.meegid.2003.10.001}}  @article{stephens:1998da,  Annote = {Summary  The {CCR5-[Delta]32} deletion obliterates the {CCR5} chemokine and the human immunodeficiency virus {(HIV)-1} coreceptor on lymphoid cells, leading to strong resistance against {HIV-1} infection and {AIDS.} A genotype survey of 4,166 individuals revealed a cline of {CCR5-[Delta]32} allele frequencies of 0\%-14\% across Eurasia, whereas the variant is absent among native African, American Indian, and East Asian ethnic groups. Haplotype analysis of 192 Caucasian chromosomes revealed strong linkage disequilibrium between {CCR5} and two microsatellite loci. By use of coalescence theory to interpret modern haplotype genealogy, we estimate the origin of the {CCR5-[Delta]32-containing} ancestral haplotype to be {\textasciitilde}700 years ago, with an estimated range of 275-1,875 years. The geographic cline of {CCR5-[Delta]32} frequencies and its recent emergence are consistent with a historic strong selective event (e.g., an epidemic of a pathogen that, like {HIV-1,} utilizes {CCR5),} driving its frequency upward in ancestral Caucasian populations.},  Author = {Stephens, J. Claiborne and Reich, David E. and Goldstein, David B. and Shin, Hyoung Doo and Smith, Michael W. and Carrington, Mary and Winkler, Cheryl and Huttley, Gavin A. and Allikmets, Rando and Schriml, Lynn and Gerrard, Bernard and Malasky, Michael and Ramos, Maria D. and Morlot, Susanne and Tzetis, Maria and Oddoux, Carole and di Giovine, Francesco S. and Nasioulas, Georgios and Chandler, David and Aseev, Michael and Hanson, Matthew and Kalaydjieva, Luba and Glavac, Damjan and Gasparini, Paolo and Kanavakis, E. and Claustres, Mireille and Kambouris, Marios and Ostrer, Harry and Duff, Gordon and Baranov, Vladislav and Sibul, Hiljar and Metspalu, Andres and Goldman, David and Martin, Nick and Duffy, David and Schmidtke, Jorg and Estivill, Xavier and {O'Brien}, Stephen J. and Dean, Michael},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1086/301867},  Issn = {0002-9297},  Journal = {The American Journal of Human Genetics},  Keywords = {{AIDS} resistance, Ancestral haplotype, Coalescence of haplotypes, Phylogenetic analysis, Short tandem-repeat polymorphism},  Month = jun,  Number = {6},  Pages = {1507--1515},  Title = {Dating the Origin of the {CCR5-[Delta]32} {AIDS-Resistance} Allele by the Coalescence of Haplotypes},  Url = {http://www.sciencedirect.com/science/article/B8JDD-4RDBM6M-12/2/9f79fd03bd3f44faba8404aef2a6c5c8},  Volume = {62},  Year = {1998},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B8JDD-4RDBM6M-12/2/9f79fd03bd3f44faba8404aef2a6c5c8},  Bdsk-Url-2 = {http://dx.doi.org/10.1086/301867}}  @article{Streftaris:2004uq,  Abstract = {We consider continuous-time stochastic compartmental models that can be applied in veterinary epidemiology to model the within-herd dynamics of infectious diseases. We focus on an extension of Markovian epidemic models, allowing the infectious period of an individual to follow a Weibull distribution, resulting in a more flexible model for many diseases. Following a Bayesian approach we show how approximation methods can be applied to design efficient MCMC algorithms with favourable mixing properties for fitting non-Markovian models to partial observations of epidemic processes. The methodology is used to analyse real data concerning a smallpox outbreak in a human population, and a simulation study is conducted to assess the effects of the frequency and accuracy of diagnostic tests on the information yielded on the epidemic process.},  Address = {338 EUSTON ROAD, LONDON NW1 3BH, ENGLAND},  Author = {Streftaris, G and Gibson, GJ},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {DOI 10.1191/1471082X04st065oa},  Isi = {000220682400004},  Isi-Recid = {134152689},  Isi-Ref-Recids = {103368257 95300111 65170366 70601182 126329392 107431130 72811647 101030461 104569679 107031825 98580464 94466653 33771207 127210831 108835391 78069508 91296799},  Journal = {Statistical Modelling},  Keywords = {Bayesian inference; diagnostic tests; Markov chain Monte Carlo; Metropolis-Hastings acceptance rate; non-Markovian model; stochastic epidemic modelling},  Month = apr,  Number = {1},  Pages = {63--75},  Publisher = {ARNOLD, HODDER HEADLINE PLC},  Times-Cited = {10},  Title = {Bayesian inference for stochastic epidemics in closed populations},  Volume = {4},  Year = {2004},  Bdsk-Url-1 = {http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Alerting&SrcApp=Alerting&DestApp=WOS&DestLinkType=FullRecord;KeyUT=000220682400004}}  @article{Strimmer:2001vn,  Abstract = {We present an intuitive visual framework, the generalized skyline plot, to explore the demographic history of sampled DNA sequences. This approach is based on a genealogy inferred from the sequences and provides a nonparametric estimate of effective population size through time. In contrast to previous related procedures, the generalized skyline plot is more applicable to cases where the underlying tree is not fully resolved and the data is not highly variable. This is achieved by the grouping of adjacent coalescent intervals. We employ a small-sample Akaike information criterion to objectively choose the optimal grouping strategy. We investigate the performance of our approach using simulation and subsequently apply it to HIV-1 sequences from central Africa and mtDNA sequences from red pandas.},  Author = {Strimmer, K and Pybus, O G},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-04 01:59:20 +0000},  Journal = {Mol Biol Evol},  Journal-Full = {Molecular biology and evolution},  Mesh = {Africa; Animals; Base Sequence; China; DNA; DNA, Mitochondrial; Data Interpretation, Statistical; Genetics, Population; HIV-1; Humans; Models, Genetic; Phylogeny; Ursidae},  Month = {12},  Number = {12},  Pages = {2298-305},  Pmid = {11719579},  Pst = {ppublish},  Title = {Exploring the demographic history of DNA sequences using the generalized skyline plot},  Volume = {18},  Year = {2001}}  @article{suchard:2009ma,  Abstract = {Motivation: Statistical phylogenetics is computationally intensive, resulting in considerable attention meted on techniques for parallelization. Codon-based models allow for independent rates of synonymous and replacement substitutions and have the potential to more adequately model the process of protein-coding sequence evolution with a resulting increase in phylogenetic accuracy. Unfortunately, due to the high number of codon states, computational burden has largely thwarted phylogenetic reconstruction under codon models, particularly at the genomic-scale. Here, we describe novel algorithms and methods for evaluating phylogenies under arbitrary molecular evolutionary models on graphics processing units {(GPUs),} making use of the large number of processing cores to efficiently parallelize calculations even for large state-size models. Results: We implement the approach in an existing Bayesian framework and apply the algorithms to estimating the phylogeny of 62 complete mitochondrial genomes of carnivores under a 60-state codon model. We see a near 90-fold speed increase over an optimized {CPU-based} computation and a {\textgreater}140-fold increase over the currently available implementation, making this the first practical use of codon models for phylogenetic inference over whole mitochondrial or microorganism genomes. Availability and implementation: Source code provided in {BEAGLE:} Broad-platform Evolutionary Analysis General Likelihood Evaluator, a cross-platform/processor library for phylogenetic likelihood computation (http://beagle-lib.googlecode.com/). We employ a {BEAGLE-implementation} using the Bayesian phylogenetics framework {BEAST} (http://beast.bio.ed.ac.uk/). Contact: [email protected]; [email protected]},  Author = {Suchard, Marc A. and Rambaut, Andrew},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-27 15:57:30 +1300},  Doi = {10.1093/bioinformatics/btp244},  Journal = {Bioinformatics},  Month = jun,  Number = {11},  Pages = {1370--1376},  Title = {Many-core algorithms for statistical phylogenetics},  Volume = {25},  Year = {2009},  Bdsk-Url-1 = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/25/11/1370},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/bioinformatics/btp244}}  @article{suzuki:2010ph,  Annote = {When multiple strains of viruses with segmented genomes co-infect a single cell, strains with novel genomic constellations may be created. This mutational process, called reassortment, has caused pandemics of influenza A virus in 1957 and 1968. Here a phylogenetic approach to detecting reassortments, which can be used even when the phylogenetic tree constructed for all strains analyzed is unreliable, is presented. A quartet of strains is examined at a time, where a phylogenetic tree is constructed for each genomic segment and the topology is compared among segments only when all quartet trees are supported with a statistical significance. The occurrence of reassortment and the segments involved in the reassortment event are inferred according to the pattern of topological difference among segments. The reassortment point for a pattern is inferred by superimposing the exterior branches of relevant quartet trees on the all-strains trees. In the analysis of {H1N1} and {H3N2} human influenza A viruses, a topological difference was observed for all pairs of genomic segments, suggesting that there is no pair of segments that has always co-segregated in reassortment during the evolutionary history of these viruses. When the reassortment point was inferred for the pattern of topological difference that was supported with the largest number of quartets for each virus, the results appeared to be mostly correct, suggesting that the method was largely reliable.},  Author = {Suzuki, Yoshiyuki},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1016/j.gene.2010.05.002},  Issn = {0378-1119},  Journal = {Gene},  Keywords = {phylogenetic tree, quartet, Reassortment, segmented genome, virus},  Number = {1-2},  Pages = {11--16},  Title = {A phylogenetic approach to detecting reassortments in viruses with segmented genomes},  Url = {http://www.sciencedirect.com/science/article/B6T39-505Y0NP-1/2/0c14c4f98adfad5f4ed95aa2014ec0e9},  Volume = {464},  Year = {2010},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6T39-505Y0NP-1/2/0c14c4f98adfad5f4ed95aa2014ec0e9},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.gene.2010.05.002}}  @article{swofford:2003pa,  Author = {Swofford, D. L.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 03:16:46 +0000},  Journal = {Massachusetts: Sinauer Associates, Sunderland},  Keywords = {bibtex-import, likelihood, parsimony, Phylogeny, phyloinformatics, Software},  Shorttitle = {{PAUP*}},  Title = {{PAUP*:} phylogenetic analysis using parsimony (* and other methods). Version 4},  Year = {2003}}  @article{Takahata:1987kx,  Abstract = {Rates of molecular evolution at some loci are more irregular than described by simple Poisson processes. Three situations under which molecular evolution would not follow simple Poisson processes are reevaluated from the viewpoint of the neutrality hypothesis: concomitant or multiple substitutions in a gene, fluctuating substitution rates in time caused by coupled effects of deleterious mutations and bottlenecks, and changes in the degree of selective constraints against a gene (neutral space) caused by successive substitutions. The common underlying assumption that these causes are lineage nonspecific excludes the case where mutation rates themselves change systematically among lineages or taxonomic groups, and severely limits the extent of variation in the number of substitutions among lineages. Even under this stringent condition, however, the third hypothesis, the fluctuating neutral space model, can generate fairly large variation. This is described by a time-dependent renewal process, which does not exhibit any episodic nature of molecular evolution. It is argued that the observed elevated variances in the number of nucleotide or amino acid substitutions do not immediately call for positive Darwinian selection in molecular evolution.},  Author = {Takahata, N},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Animals; Biological Evolution; Biometry; Models, Genetic; Stochastic Processes; Time Factors},  Month = {May},  Number = {1},  Pages = {169-79},  Pmc = {PMC1203115},  Pmid = {3596230},  Pst = {ppublish},  Title = {On the overdispersed molecular clock},  Volume = {116},  Year = {1987}}  @article{takahata:1991ge,  Abstract = {In a geographically structured population, the interplay among gene migration, genetic drift and natural selection raises intriguing evolutionary problems, but the rigorous mathematical treatment is often very difficult. Therefore several approximate formulas were developed concerning the coalescence process of neutral genes and the fixation process of selected mutations in an island model, and their accuracy was examined by computer simulation. When migration is limited, the coalescence (or divergence) time for sampled neutral genes can be described by the convolution of exponential functions, as in a panmictic population, but it is determined mainly by migration rate and the number of demes from which the sample is taken. This time can be much longer than that in a panmictic population with the same number of breeding individuals. For a selected mutation, the spreading over the entire population was formulated as a birth and death process, in which the fixation probability within a deme plays a key role. With limited amounts of migration, even advantageous mutations take a large number of generations to spread. Furthermore, it is likely that these mutations which are temporarily fixed in some demes may be swamped out again by non-mutant immigrants from other demes unless selection is strong enough. These results are potentially useful for testing quantitatively various hypotheses that have been proposed for the origin of modern human populations.},  Author = {Takahata, N.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Genetics},  Number = {2},  Pages = {585--595},  Title = {Genealogy of neutral genes and spreading of selected mutations in a geographically structured population},  Url = {http://www.scopus.com.ezproxy.auckland.ac.nz/inward/record.url?eid=2-s2.0-0025945698&partnerID=40&md5=6014dfbeabcb13874041073152fff452},  Volume = {129},  Year = {1991},  Bdsk-Url-1 = {http://www.scopus.com.ezproxy.auckland.ac.nz/inward/record.url?eid=2-s2.0-0025945698&partnerID=40&md5=6014dfbeabcb13874041073152fff452}}  @article{Takahata:1991vn,  Abstract = {The most commonly used statistical model to describe the rate constancy of molecular evolution (molecular clock) is a simple Poisson process in which the variance of the number of amino acid or nucleotide substitutions in a particular gene should be equal to the mean and henceforth the dispersion index, the ratio of the variance to the mean, should be equal to one. Recent sequence data, however, have shown that the substitutional process in molecular evolution is often considerably overdispersed and have called into question the generality of using a simple Poisson process. Several efforts have been made to develop more realistic models of molecular evolution. In this paper, I will show that the spatial (site-specific) variation in the rate of molecular evolution is an improbable cause of the overdispersion and then review various statistical models which take the temporal variation into account. Although these models do not immediately specify what the mechanisms of molecular evolution might be, they do make qualitatively different predictions and give some insight into their inference. One way to distinguish them is suggested. In addition, effects of selected substitutions that presumably occur after a major change in a molecule are quasi-quantitatively examined. It is most likely that the overdispersion of molecular clock is due either to a major molecular reconfiguration (fluctuating neutral space) led by a series of subliminal neutral changes or to selected substitutions fine-tuning a molecule after a major molecular change. Although the latter possibility, of course, violates the simplest neutrality assumption, it would not impair the neutral theory as a whole.},  Author = {Takahata, N},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Theor Popul Biol},  Journal-Full = {Theoretical population biology},  Mesh = {Biological Evolution; Humans; Models, Statistical; Molecular Biology; Poisson Distribution},  Month = {Jun},  Number = {3},  Pages = {329-44},  Pmid = {1896948},  Pst = {ppublish},  Title = {Statistical models of the overdispersed molecular clock},  Volume = {39},  Year = {1991}}  @article{takebe:2003hi,  Abstract = {Objectives: To investigate the molecular epidemiology and genetic structure of {HIV-1s} causing the epidemic in Central Myanmar and to explore the genesis of {HIV} epidemic in this area.  Design: A molecular epidemiological investigation was conducted in 1999-2000 in the city of Mandalay among high-risk populations and the structural features of circulating {HIV-1s} were analyzed.  Methods: {HIV-1} genotypes of 59 specimens were screened based on gag (p17) and env {(C2/V3)} regions. Near full-length nucleotide sequences of {HIV-1} isolates with subtype discordance were determined and their recombinant structures were characterized.  Results: Three lineages of {HIV-1} strains, including {CRF01\_AE} (27, 45.8\%), subtype B' {(Thailand} variant of subtype B) (15, 25.4\%) and subtype C (8, 13.6\%), were distributed in Mandalay, while substantial portions (9, 15.3\%) of specimens showed various patterns of subtype discordance in different regions of {HIV-1} genomes. The study on six {HIV-1} isolates with subtype discordance revealed that they were highly diverse types of unique recombinant forms {(URFs)} comprised of various combinations of three circulating subtypes. One {URF} was a particularly complex mosaic that contained 13 recombination breakpoints between three {HIV-1} subtypes. Approximately half of recombinants showed 'pseudotype' virion structures, in which the external portions of envelope glycoproteins were exchanged with different lineages of {HIV-1} strains, suggesting the potential selective advantage of 'pseudotype' viruses over parental strains.  Conclusion: The study revealed the unique geographical hot spot in Central Myanmar where extensive recombination events appeared to be taking place continually. This reflects the presence of highly exposed individuals and social networks of {HIV-1} transmission.  {(C)} 2003 Lippincott Williams \& Wilkins, Inc.},  Author = {Takebe, Yutaka and Motomura, Kazushi and Tatsumi, Masashi and Lwin, Hla Htut and Zaw, Myint and Kusagawa, Shigeru},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0269-9370},  Journal = {{AIDS}},  Keywords = {{HIV-1,} injecting drug users, molecular epidemiology, Myanmar, recombination, unique recombinant forms {(URFs)}},  Number = {14},  Title = {High prevalence of diverse forms of {HIV-1} intersubtype recombinants in Central Myanmar: geographical hot spot of extensive recombination},  Url = {http://journals.lww.com/aidsonline/Fulltext/2003/09260/High_prevalence_of_diverse_forms_of_HIV_1.9.aspx},  Volume = {17},  Year = {2003},  Bdsk-Url-1 = {http://journals.lww.com/aidsonline/Fulltext/2003/09260/High_prevalence_of_diverse_forms_of_HIV_1.9.aspx}}  @article{takehisa:2009or,  Abstract = {Western lowland gorillas {(Gorilla} gorilla gorilla) are infected with a simian immunodeficiency virus {(SIVgor)} that is closely related to chimpanzee and human immunodeficiency viruses {(SIVcpz} and {HIV-1,} respectively) in west central Africa. Although existing data suggest a chimpanzee origin for {SIVgor,} a paucity of available sequences has precluded definitive conclusions. Here, we report the molecular characterization of one partial {(BQ664)} and three full-length {(CP684,} {CP2135,} and {CP2139)} {SIVgor} genomes amplified from fecal {RNAs} of wild-living gorillas at two field sites in Cameroon. Phylogenetic analyses showed that all {SIVgor} strains clustered together, forming a monophyletic lineage throughout their genomes. Interestingly, the closest relatives of {SIVgor} were not {SIVcpzPtt} strains from west central African chimpanzees {(Pan} troglodytes troglodytes) but human viruses belonging to {HIV-1} group O. In trees derived from most genomic regions, {SIVgor} and {HIV-1} group O formed a sister clade to the {SIVcpzPtt} lineage. However, in a tree derived from 5' pol sequences ([{\textasciitilde}]900 bp), {SIVgor} and {HIV-1} group O fell within the {SIVcpzPtt} radiation. The latter was due to two {SIVcpzPtt} strains that contained mosaic pol sequences, pointing to the existence of a divergent {SIVcpzPtt} lineage that gave rise to {SIVgor} and {HIV-1} group O. Gorillas appear to have acquired this lineage at least 100 to 200 years ago. To examine the biological properties of {SIVgor,} we synthesized a full-length provirus from fecal consensus sequences. Transfection of the resulting clone {(CP2139.287)} into {293T} cells yielded infectious virus that replicated efficiently in both human and chimpanzee {CD4+} T cells and used {CCR5} as the coreceptor for viral entry. Together, these results provide strong evidence that P. t. troglodytes apes were the source of {SIVgor.} These same apes may also have spawned the group O epidemic; however, the possibility that gorillas served as an intermediary host cannot be excluded.},  Author = {Takehisa, Jun and Kraus, Matthias H. and Ayouba, Ahidjo and Bailes, Elizabeth and {Van Heuverswyn}, Fran and Decker, Julie M. and Li, Yingying and Rudicell, Rebecca S. and Learn, Gerald H. and Neel, Cecile and Ngole, Eitel Mpoudi and Shaw, George M. and Peeters, Martine and Sharp, Paul M. and Hahn, Beatrice H.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.02311-08},  Journal = {The Journal of Virology},  Month = feb,  Number = {4},  Pages = {1635--1648},  Title = {Origin and Biology of Simian Immunodeficiency Virus in {Wild-Living} Western Gorillas},  Url = {http://jvi.asm.org/cgi/content/abstract/83/4/1635},  Volume = {83},  Year = {2009},  Bdsk-Url-1 = {http://jvi.asm.org/cgi/content/abstract/83/4/1635},  Bdsk-Url-2 = {http://dx.doi.org/10.1128/JVI.02311-08}}  @article{Tanaka:2006fk,  Abstract = {Tuberculosis can be studied at the population level by genotyping strains of Mycobacterium tuberculosis isolated from patients. We use an approximate Bayesian computational method in combination with a stochastic model of tuberculosis transmission and mutation of a molecular marker to estimate the net transmission rate, the doubling time, and the reproductive value of the pathogen. This method is applied to a published data set from San Francisco of tuberculosis genotypes based on the marker IS6110. The mutation rate of this marker has previously been studied, and we use those estimates to form a prior distribution of mutation rates in the inference procedure. The posterior point estimates of the key parameters of interest for these data are as follows: net transmission rate, 0.69/year [95\% credibility interval (C.I.) 0.38, 1.08]; doubling time, 1.08 years (95\% C.I. 0.64, 1.82); and reproductive value 3.4 (95\% C.I. 1.4, 79.7). These figures suggest a rapidly spreading epidemic, consistent with observations of the resurgence of tuberculosis in the United States in the 1980s and 1990s.},  Author = {Tanaka, Mark M and Francis, Andrew R and Luciani, Fabio and Sisson, S A},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1534/genetics.106.055574},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Algorithms; Bayes Theorem; Computational Biology; Genetic Markers; Genotype; Humans; Mutation; Risk Factors; San Francisco; Tuberculosis},  Month = {Jul},  Number = {3},  Pages = {1511-20},  Pmc = {PMC1526704},  Pmid = {16624908},  Pst = {ppublish},  Title = {Using approximate Bayesian computation to estimate tuberculosis transmission parameters from genotype data},  Volume = {173},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.106.055574}}  @article{taubenberger:2005ch,  Author = {Taubenberger, Jeffery K. and Reid, Ann H. and Lourens, Raina M. and Wang, Ruixue and Jin, Guozhong and Fanning, Thomas G.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/nature04230},  Issn = {0028-0836},  Journal = {Nature},  Number = {7060},  Pages = {889--893},  Title = {Characterization of the 1918 influenza virus polymerase genes},  Url = {http://www.nature.com/doifinder/10.1038/nature04230},  Volume = {437},  Year = {2005},  Bdsk-Url-1 = {http://www.nature.com/doifinder/10.1038/nature04230},  Bdsk-Url-2 = {http://dx.doi.org/10.1038/nature04230}}  @article{Taylor:2005cq,  Abstract = {Because recombination between a pair of viral genomes can occur only when both viruses are present in the same host, genealogical evidence of recombination is influenced by the rate of viral migration between infected hosts. If superinfection is rare, then recombining viral genomes will usually be more closely related to each other than to viral genomes present in other hosts and the impact of recombination on the genealogy of a sample of viruses from different hosts may be weak. We used this relationship to estimate the relative rate of intra-subtype HIV-1 superinfection in six urban populations. Comparisons of the population recombination rates estimated from the HIV-1 sequence data with population recombination rates estimated for sets of sequences simulated using a structured coalescent process suggest that intra-subtype superinfection rates in all but one of these populations may be as high as 15\% of the corresponding infection rate. However, we caution that these estimates might be upwardly biased if variation in contact and mixing rates between infected hosts causes viral lineages to be concentrated in groups with higher than average superinfection rates.},  Author = {Taylor, Jesse E and Korber, Bette T},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.meegid.2004.07.001},  Journal = {Infect Genet Evol},  Journal-Full = {Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases},  Mesh = {Evolution, Molecular; Genetic Variation; HIV Infections; HIV-1; Humans; Models, Genetic; Molecular Epidemiology; Mutation; Recombination, Genetic; Superinfection},  Month = {Jan},  Number = {1},  Pages = {85-95},  Pmid = {15567142},  Pst = {ppublish},  Title = {HIV-1 intra-subtype superinfection rates: estimates using a structured coalescent with recombination},  Volume = {5},  Year = {2005},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.meegid.2004.07.001}}  @article{tee:2009es,  Annote = {{HIV} is capable of frequent genetic exchange through recombination. Despite the pandemic spread of {HIV-1} recombinants, their times of origin are not well understood. We investigate the epidemic history of a {HIV-1} circulating recombinant form {(CRF)} by estimating the time of the recombination event that lead to the emergence of {CRF33\_01B,} a recently described recombinant descended from {CRF01\_AE} and subtype B. The gag, pol and env genes were analyzed using a combined coalescent and relaxed molecular clock model, implemented in a Bayesian Markov chain Monte Carlo framework. Using linked genealogical trees we calculated the time interval between the common ancestor of {CRF33\_01B} and the ancestors it shares with closely related parental lineages. The recombination event that generated {CRF33\_01B} (trec) occurred sometime between 1991 and 1993, suggesting that recombination is common in the early evolutionary history of {HIV-1.} The proof-of-concept approach provides a new tool for the investigation of {HIV} molecular epidemiology and evolution.},  Author = {Tee, Kok Keng and Pybus, Oliver G. and Parker, Joe and Ng, Kee Peng and Kamarulzaman, Adeeba and Takebe, Yutaka},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {doi: DOI: 10.1016/j.virol.2009.02.020},  Issn = {0042-6822},  Journal = {Virology},  Keywords = {Coalescence, Genesis, {HIV,} recombination, Reticulate evolution},  Month = apr,  Number = {1},  Pages = {229--234},  Title = {Estimating the date of origin of an {HIV-1} circulating recombinant form},  Url = {http://www.sciencedirect.com/science/article/B6WXR-4VT17M3-5/2/b82934708b0b649c5d4690766239d00b},  Volume = {387},  Year = {2009},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6WXR-4VT17M3-5/2/b82934708b0b649c5d4690766239d00b},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.virol.2009.02.020}}  @article{templeton:2004st,  Abstract = {Nested clade phylogeographical analysis {(NCPA)} has become a common tool in intraspecific phylogeography. To evaluate the validity of its inferences, {NCPA} was applied to actual data sets with 150 strong a priori expectations, the majority of which had not been analysed previously by {NCPA.} {NCPA} did well overall, but it sometimes failed to detect an expected event and less commonly resulted in a false positive. An examination of these errors suggested some alterations in the {NCPA} inference key, and these modifications reduce the incidence of false positives at the cost of a slight reduction in power. Moreover, {NCPA} does equally well in inferring events regardless of the presence or absence of other, unrelated events. A reanalysis of some recent computer simulations that are seemingly discordant with these results revealed that {NCPA} performed appropriately in these simulated samples and was not prone to a high rate of false positives under sampling assumptions that typify real data sets. {NCPA} makes a posteriori use of an explicit inference key for biological interpretation after statistical hypothesis testing. Alternatives to {NCPA} that claim that biological inference emerges directly from statistical testing are shown in fact to use an a priori inference key, albeit implicitly. It is argued that the a priori and a posteriori approaches to intraspecific phylogeography are complementary, not contradictory. Finally, cross-validation using multiple {DNA} regions is shown to be a powerful method of minimizing inference errors. A likelihood ratio hypothesis testing framework has been developed that allows testing of phylogeographical hypotheses, extends {NCPA} to testing specific hypotheses not within the formal inference key (such as the {out-of-Africa} replacement hypothesis of recent human evolution) and integrates intra- and interspecific phylogeographical inference.},  Author = {Templeton, Alan R.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1046/j.1365-294X.2003.02041.x},  Journal = {Molecular Ecology},  Number = {4},  Pages = {789--809},  Shorttitle = {Statistical phylogeography},  Title = {Statistical phylogeography: methods of evaluating and minimizing inference errors},  Url = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1046/j.1365-294X.2003.02041.x},  Volume = {13},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org.ezproxy.auckland.ac.nz/10.1046/j.1365-294X.2003.02041.x},  Bdsk-Url-2 = {http://dx.doi.org/10.1046/j.1365-294X.2003.02041.x}}  @article{thorne:1998es,  Author = {Thorne, J. L. and Kishino, H and Painter, I. S.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 03:44:20 +0000},  Journal = {Molecular Biology and Evolution},  Number = {12},  Pages = {1647--1657},  Title = {Estimating the rate of evolution of the rate of molecular evolution},  Volume = {15},  Year = {1998},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/15/12/1647}}  @article{Toni:2009uq,  Abstract = {Approximate Bayesian computation (ABC) methods can be used to evaluate posterior distributions without having to calculate likelihoods. In this paper, we discuss and apply an ABC method based on sequential Monte Carlo (SMC) to estimate parameters of dynamical models. We show that ABC SMC provides information about the inferability of parameters and model sensitivity to changes in parameters, and tends to perform better than other ABC approaches. The algorithm is applied to several well-known biological systems, for which parameters and their credible intervals are inferred. Moreover, we develop ABC SMC as a tool for model selection; given a range of different mathematical descriptions, ABC SMC is able to choose the best model using the standard Bayesian model selection apparatus.},  Author = {Toni, Tina and Welch, David and Strelkowa, Natalja and Ipsen, Andreas and Stumpf, Michael P H},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {J R Soc Interface},  Journal-Full = {Journal of the Royal Society, Interface / the Royal Society},  Mesh = {Algorithms; Bayes Theorem; Common Cold; Communicable Diseases; Computer Simulation; Models, Biological; Models, Statistical; Monte Carlo Method},  Month = {Feb},  Number = {31},  Pages = {187-202},  Pmc = {PMC2658655},  Pmid = {19205079},  Pst = {ppublish},  Title = {Approximate Bayesian computation scheme for parameter inference and model selection in dynamical systems},  Volume = {6},  Year = {2009}}  @article{van:2006hu,  Annote = {10.1038/444164a},  Author = {{Van Heuverswyn}, Fran and Li, Yingying and Neel, Cecile and Bailes, Elizabeth and Keele, Brandon F. and Liu, Weimin and Loul, Severin and Butel, Christelle and Liegeois, Florian and Bienvenue, Yanga and Ngolle, Eitel Mpoudi and Sharp, Paul M. and Shaw, George M. and Delaporte, Eric and Hahn, Beatrice H. and Peeters, Martine},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/444164a},  Issn = {0028-0836},  Journal = {Nature},  Month = nov,  Number = {7116},  Pages = {164},  Title = {Hum2006mmunodeficiency viruses: {SIV} infection in wild gorillas},  Url = {http://dx.doi.org/10.1038/444164a},  Volume = {444},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/444164a}}  @article{van:spreadas,  Annote = {{PMID:} 14722895},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {The Journal of Infectious Diseases},  Month = jan,  Number = {2},  Pages = {292--302},  Title = {Spread of Hepatitis C Virus among European Injection Drug Users Infected with {HIV:} A Phylogenetic Analysis},  Url = {http://dx.doi.org/10.1086/380821},  Volume = {189},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1086/380821}}  @article{vanden:1996se,  Author = {Vanden Haesevelde, M.M. and Peeters, M. and Jannes, G. and Janssens, W. and Van Der Greon, G. and Sharp, P.M. and Saman, E.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0042-6822},  Journal = {Virology},  Number = {2},  Pages = {346--350},  Publisher = {Elsevier},  Title = {{Sequence analysis of a highly divergent HIV-1-related lentivirus isolated from a wild captured chimpanzee}},  Volume = {221},  Year = {1996}}  @article{Viboud:2006fk,  Abstract = {Quantifying long-range dissemination of infectious diseases is a key issue in their dynamics and control. Here, we use influenza-related mortality data to analyze the between-state progression of interpandemic influenza in the United States over the past 30 years. Outbreaks show hierarchical spatial spread evidenced by higher pairwise synchrony between more populous states. Seasons with higher influenza mortality are associated with higher disease transmission and more rapid spread than are mild ones. The regional spread of infection correlates more closely with rates of movement of people to and from their workplaces (workflows) than with geographical distance. Workflows are described in turn by a gravity model, with a rapid decay of commuting up to around 100 km and a long tail of rare longer range flow. A simple epidemiological model, based on the gravity formulation, captures the observed increase of influenza spatial synchrony with transmissibility; high transmission allows influenza to spread rapidly beyond local spatial constraints.},  Author = {Viboud, C{\'e}cile and Bj{\o}rnstad, Ottar N and Smith, David L and Simonsen, Lone and Miller, Mark A and Grenfell, Bryan T},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1125237},  Journal = {Science},  Journal-Full = {Science (New York, N.Y.)},  Mesh = {Adult; Algorithms; Child; Disease Outbreaks; Hospitalization; Humans; Incidence; Influenza A Virus, H1N1 Subtype; Influenza A Virus, H3N2 Subtype; Influenza B virus; Influenza, Human; Models, Statistical; Population Density; Seasons; Stochastic Processes; Time Factors; Travel; United States; Workplace},  Month = {Apr},  Number = {5772},  Pages = {447-51},  Pmid = {16574822},  Pst = {ppublish},  Title = {Synchrony, waves, and spatial hierarchies in the spread of influenza},  Volume = {312},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1125237}}  @article{Vijaykrishna:2008fc,  Abstract = {The highly pathogenic avian influenza (HPAI) H5N1 virus lineage has undergone extensive genetic reassortment with viruses from different sources to produce numerous H5N1 genotypes, and also developed into multiple genetically distinct sublineages in China. From there, the virus has spread to over 60 countries. The ecological success of this virus in diverse species of both poultry and wild birds with frequent introduction to humans suggests that it is a likely source of the next human pandemic. Therefore, the evolutionary and ecological characteristics of its emergence from wild birds into poultry are of considerable interest. Here, we apply the latest analytical techniques to infer the early evolutionary dynamics of H5N1 virus in the population from which it emerged (wild birds and domestic poultry). By estimating the time of most recent common ancestors of each gene segment, we show that the H5N1 prototype virus was likely introduced from wild birds into poultry as a non-reassortant low pathogenic avian influenza H5N1 virus and was not generated by reassortment in poultry. In contrast, more recent H5N1 genotypes were generated locally in aquatic poultry after the prototype virus (A/goose/Guangdong/1/96) introduction occurred, i.e., they were not a result of additional emergence from wild birds. We show that the H5N1 virus was introduced into Indonesia and Vietnam 3-6 months prior to detection of the first outbreaks in those countries. Population dynamics analyses revealed a rapid increase in the genetic diversity of A/goose/Guangdong/1/96 lineage viruses from mid-1999 to early 2000. Our results suggest that the transmission of reassortant viruses through the mixed poultry population in farms and markets in China has selected HPAI H5N1 viruses that are well adapted to multiple hosts and reduced the interspecies transmission barrier of those viruses.},  Author = {Vijaykrishna, Dhanasekaran and Bahl, Justin and Riley, Steven and Duan, Lian and Zhang, Jin Xia and Chen, Honglin and Peiris, J S Malik and Smith, Gavin J D and Guan, Yi},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.ppat.1000161},  Journal = {PLoS Pathog},  Journal-Full = {PLoS pathogens},  Mesh = {Animals; Birds; Communicable Diseases, Emerging; Evolution; Genotype; Humans; Influenza A Virus, H5N1 Subtype; Phylogeny; Poultry; Species Specificity; Zoonoses},  Number = {9},  Pages = {e1000161},  Pmc = {PMC2533123},  Pmid = {18818732},  Pst = {epublish},  Title = {Evolutionary dynamics and emergence of panzootic H5N1 influenza viruses},  Volume = {4},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.ppat.1000161}}  @article{Volz:2009pr,  Abstract = {We present a formalism for unifying the inference of population size from genetic sequences and mathematical models of infectious disease in populations. Virus phylogenies have been used in many recent studies to infer properties of epidemics. These approaches rely on coalescent models that may not be appropriate for infectious diseases. We account for phylogenetic patterns of viruses in susceptible-infected (SI), susceptible-infected-susceptible (SIS), and susceptible-infected-recovered (SIR) models of infectious disease, and our approach may be a viable alternative to demographic models used to reconstruct epidemic dynamics. The method allows epidemiological parameters, such as the reproductive number, to be estimated directly from viral sequence data. We also describe patterns of phylogenetic clustering that are often construed as arising from a short chain of transmissions. Our model reproduces the moments of the distribution of phylogenetic cluster sizes and may therefore serve as a null hypothesis for cluster sizes under simple epidemiological models. We examine a small cross-sectional sample of human immunodeficiency (HIV)-1 sequences collected in the United States and compare our results to standard estimates of effective population size. Estimated prevalence is consistent with estimates of effective population size and the known history of the HIV epidemic. While our model accurately estimates prevalence during exponential growth, we find that periods of decline are harder to identify.},  Author = {Volz, Erik M and Kosakovsky Pond, Sergei L and Ward, Melissa J and Leigh Brown, Andrew J and Frost, Simon D W},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1534/genetics.109.106021},  Journal = {Genetics},  Journal-Full = {Genetics},  Mesh = {Communicable Diseases; Disease Outbreaks; Disease Susceptibility; Evolution, Molecular; HIV; HIV Infections; Models, Biological; Phylogeny; Virus Diseases; Viruses},  Month = {Dec},  Number = {4},  Pages = {1421-30},  Pmc = {PMC2787429},  Pmid = {19797047},  Pst = {ppublish},  Title = {Phylodynamics of infectious disease epidemics},  Volume = {183},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.109.106021}}  @article{wallace:2007st,  Author = {Wallace, R.G. and HoDac, H.M. and Lathrop, R.H. and Fitch, W.M.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Proceedings of the National Academy of Sciences},  Number = {11},  Pages = {4473},  Publisher = {National Acad Sciences},  Title = {{A statistical phylogeography of influenza A H5N1}},  Volume = {104},  Year = {2007}}  @article{Wallinga:2007ve,  Abstract = {Mathematical models of transmission have become invaluable management tools in planning for the control of emerging infectious diseases. A key variable in such models is the reproductive number R. For new emerging infectious diseases, the value of the reproductive number can only be inferred indirectly from the observed exponential epidemic growth rate r. Such inference is ambiguous as several different equations exist that relate the reproductive number to the growth rate, and it is unclear which of these equations might apply to a new infection. Here, we show that these different equations differ only with respect to their assumed shape of the generation interval distribution. Therefore, the shape of the generation interval distribution determines which equation is appropriate for inferring the reproductive number from the observed growth rate. We show that by assuming all generation intervals to be equal to the mean, we obtain an upper bound to the range of possible values that the reproductive number may attain for a given growth rate. Furthermore, we show that by taking the generation interval distribution equal to the observed distribution, it is possible to obtain an empirical estimate of the reproductive number.},  Author = {Wallinga, J and Lipsitch, M},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Proc Biol Sci},  Journal-Full = {Proceedings. Biological sciences / The Royal Society},  Mesh = {Cohort Effect; Disease Outbreaks; Humans; Influenza, Human; Models, Biological},  Month = {Feb},  Number = {1609},  Pages = {599-604},  Pmc = {PMC1766383},  Pmid = {17476782},  Pst = {ppublish},  Title = {How generation intervals shape the relationship between growth rates and reproductive numbers},  Volume = {274},  Year = {2007}}  @article{webby:2000ev,  Abstract = {During 1998, severe outbreaks of influenza were observed in four swine herds in the United States. This event was unique because the causative agents, {H3N2} influenza viruses, are infrequently isolated from swine in North America. Two antigenically distinct reassortant viruses {(H3N2)} were isolated from infected animals: a double-reassortant virus containing genes similar to those of human and swine viruses, and a triple-reassortant virus containing genes similar to those of human, swine, and avian influenza viruses {(N.} N. Zhou, D. A. Senne, J. S. Landgraf, S. L. Swenson, G. Erickson, K. Rossow, L. Liu, {K.-J.} Yoon, S. Krauss, and R. G. Webster, J. Virol. 73:8851-8856, 1999). Because the {U.S.} pig population was essentially naive in regard to {H3N2} viruses, it was important to determine the extent of viral spread. Hemagglutination inhibition {(HI)} assays of 4,382 serum samples from swine in 23 states indicated that 28.3\% of these animals had been exposed to classical swine-like {H1N1} viruses and 20.5\% had been exposed to the triple-reassortant-like {H3N2} viruses. The {HI} data suggested that viruses antigenically related to the double-reassortant {H3N2} virus have not become widespread in the {U.S.} swine population. The seroreactivity levels in swine serum samples and the nucleotide sequences of six additional 1999 isolates, all of which were of the triple-reassortant genotype, suggested that {H3N2} viruses containing avian {PA} and {PB2} genes had spread throughout much of the country. These avian-like genes cluster with genes from North American avian viruses. The worldwide predominance of swine viruses containing an avian-like internal gene component suggests that these genes may confer a selective advantage in pigs. Analysis of the 1999 swine {H3N2} isolates showed that the internal gene complex of the triple-reassortant viruses was associated with three recent phylogenetically distinct human-like hemagglutinin {(HA)} molecules. Acquisition of {HA} genes from the human virus reservoir will significantly affect the efficacy of the current swine {H3N2} vaccines. This finding supports continued surveillance of {U.S.} swine populations for influenza virus activity.},  Author = {Webby, Richard J. and Swenson, Sabrina L. and Krauss, Scott L. and Gerrish, Philip J. and Goyal, Sagar M. and Webster, Robert G.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1128/JVI.74.18.8243-8251.2000},  Journal = {The Journal of Virology},  Month = sep,  Number = {18},  Pages = {8243--8251},  Title = {Evolution of Swine {H3N2} Influenza Viruses in the United States},  Url = {http://jvi.asm.org/cgi/content/abstract/74/18/8243},  Volume = {74},  Year = {2000},  Bdsk-Url-1 = {http://jvi.asm.org/cgi/content/abstract/74/18/8243},  Bdsk-Url-2 = {http://dx.doi.org/10.1128/JVI.74.18.8243-8251.2000}}  @article{Wei:1995ly,  Abstract = {The dynamics of HIV-1 replication in vivo are largely unknown yet they are critical to our understanding of disease pathogenesis. Experimental drugs that are potent inhibitors of viral replication can be used to show that the composite lifespan of plasma virus and virus-producing cells is remarkably short (half-life approximately 2 days). Almost complete replacement of wild-type virus in plasma by drug-resistant variants occurs after fourteen days, indicating that HIV-1 viraemia is sustained primarily by a dynamic process involving continuous rounds of de novo virus infection and replication and rapid cell turnover.},  Author = {Wei, X and Ghosh, S K and Taylor, M E and Johnson, V A and Emini, E A and Deutsch, P and Lifson, J D and Bonhoeffer, S and Nowak, M A and Hahn, B H},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1038/373117a0},  Journal = {Nature},  Journal-Full = {Nature},  Mesh = {Antiviral Agents; Base Sequence; CD4 Lymphocyte Count; CD4-Positive T-Lymphocytes; Cell Survival; DNA, Viral; Drug Resistance, Microbial; Genotype; HIV Infections; HIV Protease Inhibitors; HIV Reverse Transcriptase; HIV-1; Humans; Leukocytes, Mononuclear; Molecular Sequence Data; Mutation; Phenotype; RNA, Viral; RNA-Directed DNA Polymerase; Reverse Transcriptase Inhibitors; Viremia; Virus Replication},  Month = {Jan},  Number = {6510},  Pages = {117-22},  Pmid = {7529365},  Pst = {ppublish},  Title = {Viral dynamics in human immunodeficiency virus type 1 infection},  Volume = {373},  Year = {1995},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/373117a0}}  @article{Welch2005,  Annote = {We model the genealogies of coupled haploid host-virus populations. Hosts reproduce and replace other hosts as in the Moran model. The virus can be transmitted between individuals of the same and succeeding generations. The epidemic model allows a selective advantage for susceptible over infected hosts. The coupled host-virus ancestry of a sample of hosts is embedded in a branching and coalescing structure that we call the Ancestral Infection and Selection Graph, a direct analogue to the Ancestral Selection Graph of Krone and Neuhauser [1997. Theoret. Population Biol. 51, 210-237]. We prove this and discuss various special cases. We show that the inter-host viral genealogy is a scaled coalescent. Using simulations, we compare the viral genealogy under this model to earlier published models and investigate the estimatability of the selection and infectious contact rates. We use simulations to compare the persistence of the disease with the time to the ultimate ancestor.},  Author = {Welch, David and Nicholls, Geoff K. and Rodrigo, Allen G. and Solomon, Wiremu},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2014-07-06 01:01:07 +0000},  Doi = {doi: DOI: 10.1016/j.tpb.2005.03.003},  Issn = {0040-5809},  Journal = {Theoretical Population Biology},  Keywords = {Ancestral selection graph, Coalescent, Epidemiology, Host-virus genealogy, Moran model, Population genetics},  Month = jul,  Number = {1},  Pages = {65--75},  Title = {Integrating genealogy and epidemiology: The ancestral infection and selection graph as a model for reconstructing host virus histories},  Url = {http://www.sciencedirect.com/science/article/B6WXD-4G94HM9-2/2/0a9c431ab39a017d7a200aa5d24952c7},  Volume = {68},  Year = {2005},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/B6WXD-4G94HM9-2/2/0a9c431ab39a017d7a200aa5d24952c7},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.tpb.2005.03.003}}  @article{welch2011statistical,  Author = {Welch, D. and Bansal, S. and Hunter, D.R.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {1755-4365},  Journal = {Epidemics},  Number = {1},  Pages = {38--45},  Publisher = {Elsevier},  Title = {Statistical inference to advance network models in epidemiology},  Volume = {3},  Year = {2011}}  @article{wertheim:????re,  Abstract = {In 1977, {H1N1} influenza A virus reappeared after a 20-year absence. Genetic analysis indicated that this strain was missing decades of nucleotide sequence evolution, suggesting an accidental release of a frozen laboratory strain into the general population. Recently, this strain and its descendants were included in an analysis attempting to date the origin of pandemic influenza virus without accounting for the missing decades of evolution. Here, we investigated the effect of using viral isolates with biologically unrealistic sampling dates on estimates of divergence dates. Not accounting for missing sequence evolution produced biased results and increased the variance of date estimates of the most recent common ancestor of the re-emergent lineages and across the entire phylogeny. Reanalysis of the {H1N1} sequences excluding isolates with unrealistic sampling dates indicates that the 1977 re-emergent lineage was circulating for approximately one year before detection, making it difficult to determine the geographic source of reintroduction. We suggest that a new method is needed to account for viral isolates with unrealistic sampling dates.},  Author = {Wertheim, Joel O.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.pone.0011184},  Journal = {{PLoS} One},  Number = {6},  Title = {The {Re-Emergence} of {H1N1} Influenza Virus in 1977: A Cautionary Tale for Estimating Divergence Times Using Biologically Unrealistic Sampling Dates},  Volume = {5},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pone.0011184}}  @article{wertheim:2007ch,  Abstract = {While the circumstances surrounding the origin and spread of {HIV} are becoming clearer, the particulars of the origin of simian immunodeficiency virus {(SIV)} are still unknown. Specifically, the age of {SIV,} whether it is an ancient or recent infection, has not been resolved. Although many instances of cross-species transmission of {SIV} have been documented, the similarity between the African green monkey {(AGM)} and {SIVagm} phylogenies has long been held as suggestive of ancient codivergence between {SIVs} and their primate hosts. Here, we present well-resolved phylogenies based on full-length {AGM} mitochondrial genomes and seven previously published {SIVagm} genomes; these allowed us to perform the first rigorous phylogenetic test to our knowledge of the hypothesis that {SIVagm} codiverged with the {AGMs.} Using the {Shimodaira--Hasegawa} test, we show that the {AGM} mitochondrial genomes and {SIVagm} did not evolve along the same topology. Furthermore, we demonstrate that the {SIVagm} topology can be explained by a pattern of west-to-east transmission of the virus across existing {AGM} geographic ranges. Using a relaxed molecular clock, we also provide a date for the most recent common ancestor of the {AGMs} at approximately 3 million years ago. This study substantially weakens the theory of ancient {SIV} infection followed by codivergence with its primate hosts.},  Author = {Wertheim, Joel O and Worobey, Michael},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1371/journal.ppat.0030095},  Issn = {1553-7366},  Journal = {{PLoS} Pathogens},  Month = jul,  Note = {{PMID:} 17616975 {PMCID:} 1904472},  Number = {7},  Title = {A Challenge to the Ancient Origin of {SIVagm} Based on African Green Monkey Mitochondrial Genomes},  Volume = {3},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.ppat.0030095}}  @article{wertheim:2009da,  Abstract = {{HIV/AIDS} continues to be a major health problem worldwide. An understanding of the evolution of {HIV} in humans may be greatly improved by detailed knowledge of its predecessor, simian immunodeficiency virus {(SIV),} in non-human primates. While {HIV} causes {AIDS} in humans, {SIV} generally produces a benign infection in its natural hosts. This avirulence is often attributed to coevolution between the virus and its host, possibly due to codivergence over millions of years. Here, we provide a temporal reference for evolution of {SIV} in its natural primate hosts. Using state-of-the-art molecular clock dating techniques, we estimate the time of most recent common ancestor for {SIV} in sooty mangabeys and chimpanzees at 1809 (1729{\^a}€``1875) and 1492 (1266{\^a}€``1685), respectively. These ages indicate that {SIV} may have infected these natural hosts for only hundreds of years before giving rise to {HIV.} This short duration suggests that viral{\^a}€``host coevolution over millions of years is not a likely explanation for the widespread avirulence of {SIV.} Finally, despite differences between {SIV} and {HIV} in host biology and viral pathogenicity, we have found clear and direct evidence that {SIV} evolves at a rapid rate in its natural hosts, an evolutionary rate that is indistinguishable from that of {HIV} in humans.},  Author = {Wertheim, Joel O. and Worobey, Michael},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {{PLoS} Comput Biol},  Month = may,  Number = {5},  Pages = {e1000377},  Title = {Dating the Age of the {SIV} Lineages That Gave Rise to {HIV-1} and {HIV-2}},  Url = {http://dx.doi.org/10.1371%2Fjournal.pcbi.1000377},  Volume = {5},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.1000377}}  @article{wertheim:2010re,  Author = {Wertheim, J.O.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {PLoS ONE},  Number = {6},  Pages = {e11184},  Publisher = {Public Library of Science},  Title = {{The Re-Emergence of H1N1 Influenza Virus in 1977: A Cautionary Tale for Estimating Divergence Times Using Biologically Unrealistic Sampling Dates}},  Volume = {5},  Year = {2010}}  @article{worobey:2001no,  Author = {Worobey, Michael},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Molecular Biology and Evolution},  Number = {8},  Pages = {1425 --1434},  Title = {A Novel Approach to Detecting and Measuring Recombination: New Insights into Evolution in Viruses, Bacteria, and Mitochondria},  Url = {http://mbe.oxfordjournals.org/content/18/8/1425.abstract},  Volume = {18},  Year = {2001},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/content/18/8/1425.abstract}}  @article{worobey:2004or,  Author = {Worobey, M. and Santiago, M.L. and Keele, B.F. and Ndjango, J.B.N. and Joy, J.B. and Labama, B.L. and Dhed'a, B.D. and Rambaut, A. and Sharp, P.M. and Shaw, G.M. and others},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0028-0836},  Journal = {Nature},  Number = {6985},  Pages = {820},  Publisher = {Nature Publishing Group},  Title = {{Origin of AIDS: contaminated polio vaccine theory refuted}},  Volume = {428},  Year = {2004}}  @article{worobey:2008di,  Annote = {10.1038/nature07390},  Author = {Worobey, Michael and Gemmel, Marlea and Teuwen, Dirk E. and Haselkorn, Tamara and Kunstman, Kevin and Bunce, Michael and Muyembe, {Jean-Jacques} and Kabongo, {Jean-Marie} M. and Kalengayi, Raphael M. and Marck, Eric Van and Gilbert, M. Thomas P. and Wolinsky, Steven M.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-09-27 23:30:05 +1300},  Doi = {10.1038/nature07390},  Issn = {0028-0836},  Journal = {Nature},  Month = oct,  Number = {7213},  Pages = {661--664},  Title = {Direct evidence of extensive diversity of {HIV-1} in Kinshasa by 1960},  Volume = {455},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature07390}}  @article{worobey:2010is,  Abstract = {Simian immunodeficiency virus {(SIV)} lineages have been identified that are endemic to Bioko Island. The time the island formed offers a geological time scale calibration point for dating the most recent common ancestor of {SIV.} The Bioko viruses cover the whole range of {SIV} genetic diversity, and each Bioko {SIV} clade is most closely related to viruses circulating in hosts of the same genus on the African mainland rather than to {SIVs} of other Bioko species. Our phylogeographic approach establishes that {SIV} is ancient and at least 32,000 years old. Our conservative calibration point and analyses of gene sequence saturation and dating bias suggest it may be much older.},  Author = {Worobey, Michael and Telfer, Paul and Souquiere, Sandrine and Hunter, Meredith and Coleman, Clint A. and Metzger, Michael J. and Reed, Patricia and Makuwa, Maria and Hearn, Gail and Honarvar, Shaya and Roques, Pierre and Apetrei, Cristian and Kazanji, Mirdad and Marx, Preston A.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1126/science.1193550},  Journal = {Science},  Month = sep,  Number = {5998},  Pages = {1487},  Title = {Island Biogeography Reveals the Deep History of {SIV}},  Url = {http://www.sciencemag.org.ezproxy.auckland.ac.nz/cgi/content/abstract/329/5998/1487},  Volume = {329},  Year = {2010},  Bdsk-Url-1 = {http://www.sciencemag.org.ezproxy.auckland.ac.nz/cgi/content/abstract/329/5998/1487},  Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.1193550}}  @article{Wright:1931ev,  Author = {Wright, S.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {Genetics},  Number = {2},  Pages = {97--159},  Title = {{Evolution in Mendelian populations}},  Volume = {16},  Year = {1931}}  @article{yang:1994ma,  Author = {Yang, Ziheng},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1007/BF00160154},  Journal = {Journal of Molecular Evolution},  Number = {3},  Pages = {306--314},  Title = {Maximum likelihood phylogenetic estimation from {DNA} sequences with variable rates over sites: Approximate methods},  Url = {http://dx.doi.org/10.1007/BF00160154},  Volume = {39},  Year = {1994},  Bdsk-Url-1 = {http://dx.doi.org/10.1007/BF00160154}}  @article{Yip:2009ys,  Abstract = {Severe Acute Respiratory Syndrome (SARS) is a respiratory disease caused by a zoonotic coronavirus (CoV) named SARS-CoV (SCoV), which rapidly swept the globe after its emergence in rural China during late 2002. The origins of SCoV have been mysterious and controversial, until the recent discovery of SARS-like CoV (SLCoV) in bats and the proposal of bats as the natural reservior of the Coronaviridae family. In this article, we focused on discussing how phylogenetics contributed to our understanding towards the emergence and transmission of SCoV. We first reviewed the epidemiology of SCoV from a phylogenetic perspective and discussed the controversies over its phylogenetic origins. Then, we summarized the phylogenetic findings in relation to its zoonotic origins and the proposed inter-species viral transmission events. Finally, we also discussed how the discoveries of SCoV and SLCoV expanded our knowledge on the evolution of the Coronaviridae family as well as its implications on the possible future re-emergence of SCoV.},  Author = {Yip, Chi Wai and Hon, Chung Chau and Shi, Mang and Lam, Tommy Tsan-Yuk and Chow, Ken Yan-Ching and Zeng, Fanya and Leung, Frederick Chi-Ching},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1016/j.meegid.2009.09.015},  Journal = {Infect Genet Evol},  Journal-Full = {Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases},  Mesh = {Animals; Coronavirus; Disease Reservoirs; Evolution, Molecular; Genetic Variation; Genome, Viral; Humans; Phylogeny; SARS Virus; Severe Acute Respiratory Syndrome},  Month = {Dec},  Number = {6},  Pages = {1185-96},  Pmid = {19800030},  Pst = {ppublish},  Title = {Phylogenetic perspectives on the epidemiology and origins of SARS and SARS-like coronaviruses},  Volume = {9},  Year = {2009},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.meegid.2009.09.015}}  @article{yusim:2001us,  Author = {Yusim, K. and Peeters, M. and Pybus, O.G. and Bhattacharya, T. and Korber, B.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Issn = {0962-8436},  Journal = {Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences},  Number = {1410},  Pages = {855},  Publisher = {The Royal Society},  Title = {{Using human immunodeficiency virus type 1 sequences to infer historical features of the acquired immune deficiency syndrome epidemic and human immunodeficiency virus evolution}},  Volume = {356},  Year = {2001}}  @article{zhang:????ro,  Author = {Zhang, Ming and Foley, Brian and Schultz, {Anne-Kathrin} and Macke, Jennifer P and Bulla, Ingo and Stanke, Mario and Morgenstern, Burkhard and Korber, Bette and Leitner, Thomas},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Doi = {10.1186/1742-4690-7-25},  Note = {{PMID:} 20331894 {PMCID:} 2855530},  Pages = {25--25},  Title = {The role of recombination in the emergence of a complex and dynamic {HIV} epidemic},  Volume = {7},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1742-4690-7-25}}  @article{zimmer:2009hi,  Author = {Zimmer, S.M. and Burke, D.S.},  Date-Added = {2011-04-22 15:18:57 +1200},  Date-Modified = {2011-04-22 15:18:57 +1200},  Journal = {New England Journal of Medicine},  Publisher = {Mass Med Soc},  Title = {{Historical perspective--Emergence of influenza A (H1N1) viruses}},  Year = {2009}}  @article{A.Zanotto,  Author = {de A. Zanotto, P. M. and Gould, E. A. and Gao, G. F. and Harvey, P. H. and Holmes, E. C.},  Date-Modified = {2014-07-06 03:57:38 +0000},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {548--553},  Title = {Population dynamics of flaviviruses revealed by molecular phylogeny},  Volume = {93}}  @article{Aach2001,  Author = {Aach, J. and Church, G.M.},  Journal = {Bioinformatics},  Notes = {expression},  Pages = {495--508},  Title = {Aligning gene expression time series with time warping algorithms},  Volume = {17},  Year = {2001}}  @article{Adachi1996,  Author = {Adachi, J. and Hasegawa, M.},  Journal = {Journal of Molecular Evolution},  Pages = {459--468},  Title = {Model of amino acid substitution in proteins encoded by mitochondrial DNA},  Volume = {42},  Year = {1996}}  @article{Adeleke1996,  Author = {Adeleke, A. and Prucklet, J. and Benson, R. and Rowbotham, T. and Halablab, M. and Fields, B.},  Journal = {Emerging Infectious Diseases},  Pages = {225--230},  Title = {Legionella-like amebal pathogens -- phylogenetic status and possible role in respiratory disease},  Volume = {2},  Year = {1996}}  @article{Agapow2002,  Author = {Agapow, P. and Purvis, A.},  Journal = {Systematic Biology},  Pages = {866--872},  Title = {Power of eight tree shape statistics to detect nonrandom diversification: a comparison by simulation of two models of cladogenesis},  Volume = {51},  Year = {2002}}  @article{Aguilar2000,  Author = {Aguilar, O. and West, M.},  Journal = {Journal of Business and Economic Statistics},  Pages = {338--357},  Title = {Bayesian dynamic factor models and portfolio allocation},  Volume = {18},  Year = {2000}}  @article{Ai2003,  Author = {Ai, Bao-Quan and Wang, Xian-Ju and Liu, Guo-Tao and Liu, Liang-Gang},  Doi = {10.1103/PhysRevE.67.022903},  Journal = {Phys. Rev. E},  Month = {Feb},  Number = {2},  Numpages = {3},  Pages = {022903},  Publisher = {American Physical Society},  Title = {Correlated noise in a logistic growth model},  Volume = {67},  Year = {2003},  Bdsk-Url-1 = {http://dx.doi.org/10.1103/PhysRevE.67.022903}}  @article{Albert1993,  Author = {Albert, J. and Chib, S.},  Journal = {Journal of the American Statistical Association},  Pages = {657--667},  Title = {Bayesian regression analysis of binary and polychotomous response data},  Volume = {88},  Year = {1993}}  @article{Aldous2001,  Author = {Aldous, D.J.},  Journal = {Statistical Science},  Pages = {23--34},  Title = {Stochastic models and descriptive statistics for phylogenetic trees, from Yule to today},  Volume = {16},  Year = {2001}}  @incollection{Aldous1996,  Author = {Aldous, D.},  Booktitle = {Random Discrete Structures,\},  Editors = {D. Aldous and P. Pemantle},  Notes = {tree shape},  Pages = {1--18},  Publisher = {Springer (IMA Volumes Math.\ Appl.\ 76)},  Title = {Probability distributions on cladograms},  Year = {1996}}  @book{Aldousinpreparation,  Address = {http://stat-www.berkeley.edu/users/aldous/RWG/book.html},  Author = {Aldous, D. and Fill, J.},  Publisher = {University of California, Berkeley, Department of Statistics},  Title = {Reversible Markov Chains and Random Walks on Graphs},  Year = {in preparation}}  @article{Allard1996,  Author = {Allard, M.W. and Carpenter, J.M.},  Journal = {Cladistics},  Pages = {183--198},  Title = {On weighting and congruence},  Volume = {12},  Year = {1996}}  @article{Allard1999,  Author = {Allard, M.W. and Farris, J.S. and Carpenter, J.M.},  Journal = {Cladistics},  Pages = {75--84},  Title = {Congruence among mammalian mitochondrial genes},  Volume = {15},  Year = {1999}}  @article{Allen2001,  Author = {Allen, B.L. and Steel, M.},  Journal = {Annals of Combinatorics},  Pages = {1--15},  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By deriving stochastic analogues to difference  equations from first principles, we show that the form of these models  depends on whether noise in the population process is demographic  or environmental. When noise is demographic, we argue that variance  around the expectation is proportional to the expectation. When noise  is environmental the variance depends in a non-trivial way on how  variation enters into model parameters, but we argue that if the  environment affects the population multiplicatively then variance  is proportional to the square of the expectation. We compare various  stochastic analogues of the Ricker map model by fitting them, using  maximum likelihood estimation, to data generated from an individual-based  model and the weevil data of Utida. Our demographic models are significantly  better than our environmental models at fitting noise generated by  population processes where noise is mainly demographic. However,  the traditionally chosen stochastic analogues to deterministic models--additive  normally distributed noise and multiplicative lognormally distributed  noise--generally fit all data sets well. Thus, the form of the variance  does play a role in the fitting of models to ecological time series,  but may not be important in practice as first supposed.},  Address = {Mathematics Department, Umea University, Sweden. [email protected]},  Au = {Brannstrom, A and Sumpter, DJ},  Author = {Brannstrom, A and Sumpter, D J T},  Da = {20060502},  Date-Added = {2008-04-13 17:20:00 +1200},  Date-Modified = {2008-04-13 17:31:58 +1200},  Dcom = {20061005},  Dep = {20060310},  Doi = {10.1016/j.tpb.2006.01.006},  Edat = {2006/03/15 09:00},  Issn = {0040-5809 (Print)},  Jid = {0256422},  Journal = {Theor Popul Biol},  Jt = {Theoretical population biology},  Language = {eng},  Lr = {20061115},  Mhda = {2006/10/06 09:00},  Number = {4},  Own = {NLM},  Pages = {442--451},  Pii = {S0040-5809(06)00014-1},  Pl = {United States},  Pmid = {16530798},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Theor Popul Biol. 2006 Jun;69(4):442-51. Epub 2006 Mar 10.},  Stat = {MEDLINE},  Title = {Stochastic analogues of deterministic single-species population models.},  Volume = {69},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tpb.2006.01.006}}  @article{Breiman1995,  Author = {Breiman, L.},  Journal = {Technometrics},  Pages = {373--384},  Title = {Better subset regression using nonnegative garrote},  Volume = {37},  Year = {1995}}  @article{Britten2002,  Author = {Britten, R.J.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Notes = {indel},  Pages = {13633--13635},  Title = {Divergence between samples of chimpanzee and human DNA sequences is 5\%, counting indels},  Volume = {99},  Year = {2002}}  @article{Britten1969,  Author = {Britten, R.J. and Davidson, E.H.},  Journal = {Science},  Notes = {expression},  Pages = {349--357},  Title = {Gene regulation for higher cells: a theory},  Volume = {165},  Year = {1969}}  @article{Britten2003,  Author = {Britten, R.J. and Rowen, L. and Williams, J. and Cameron, R.A.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Notes = {indel},  Pages = {4661-4665},  Title = {Majority of divergence between closely related DNA samples is due to indels},  Volume = {100},  Year = {2003}}  @article{Bromham2003,  Author = {Bromham, L.},  Journal = {Palenontologia Electronica},  Pages = {1.2E},  Title = {Into focus, molecular dates for the Cambrian explosion: is the light at the end of the tunnel an oncoming train?},  Volume = {9},  Year = {2003}}  @article{Bromham2003a,  Author = {Bromham, L. and Penny, D.},  Journal = {Nature Reviews Genetics},  Notes = {relaxed clocks},  Pages = {216--224},  Title = {The modern molecular clock},  Volume = {4},  Year = {2003}}  @article{Bromham2004,  Author = {Bromham, L. and Woolfit, M.},  Journal = {Syst Biol},  Notes = {relaxed clocks},  Pages = {758--766},  Title = {Explosive radiations and the reliability of molecular clocks: island endemic radiations as a test case},  Volume = {53},  Year = {2004}}  @article{Brooks1998,  Author = {Brooks, S.P. and Gelman, A.},  Journal = {Journal of Computational and Graphical Statistics},  Pages = {434--455},  Title = {Assessing convergence of Markov chain Monte Carlo algorithms},  Volume = {7},  Year = {1998}}  @incollection{Brooks1999,  Address = {New York, NY},  Author = {Brooks, S. 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While the mathematical theory of such processes  is very well-developed, they may be difficult to work with when attempting  to estimate parameters or expected times to extinction. Hence, we  focus on diffusion and other approximations to these models, presenting  new and recent developments in parameter estimation for density dependent  processes, and the calculation of extinction times for processes  subject to catastrophes. We illustrate these and other methods using  data from simulated and real time series. We give particular attention  to a procedure, due to Ross et al. [Ross, J.V., Taimre, T., Pollett,  P.K. On parameter estimation in population models, Theor. Popul.  Biol., in press], for estimating the parameters of the stochastic  SIS logistic model, and demonstrate ways in which these parameters  may be used to estimate expected extinction times. Although the stochastic  SIS logistic model is strictly density dependent and allows only  for birth and death events, it nonetheless may be used to predict  extinction times with some accuracy even for populations that are  only weakly density dependent, or that are subject to catastrophes.  (c) 2006 Elsevier B.V. All rights reserved.},  Author = {Cairns, B. J. and Ross, J. V. and Taimre, T.},  Date-Added = {2008-03-28 15:41:59 +1300},  Date-Modified = {2008-03-28 15:43:09 +1300},  Doi = {DOI 10.1016/j.ecolmodel.2006.07.018},  Journal = {Ecological Modelling},  Keywords = {stochastic logistic; extinction; population model; parameter estimation; catastrophes},  Pages = {19-26},  Timescited = {0},  Title = {A comparison of models for predicting population persistence},  Volume = {201},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ecolmodel.2006.07.018}}  @article{Caldeira2000,  Author = {Caldeira, S. and de Villers, E.-M. and Tommasino, M.},  Journal = {Oncogene},  Notes = {HPV},  Pages = {821--826},  Title = {Human papillomavirus E7 proteins stimulate proliferation independently of their ability to associate with retinoblastoma protein},  Volume = {19},  Year = {2000}}  @article{Caldeira2003,  Author = {Caldeira, S. and Zehbe, I. and Accardia, R. and Malanchi, I. and Dong, W. and Giarre, M. and de Villiers, E.-M. and Filotico, R. and Boukamp, P. and Tommasino, M.},  Journal = {Journal of Virology},  Notes = {HPV},  Pages = {2195--2206},  Title = {The E6 and E7 proteins of the cutaneous human papillomavirus type 38 display transforming properties},  Volume = {77},  Year = {2003}}  @article{Campbell2005,  Author = {Campbell, T.B. and Shulman, N.S. and Johnson, S.C. and Zolopa, A.R. and Young, R.K. and Bushman, L. and Fletcher, C.V. and Lanier, E.R. and Merigan, T.C. and Kuritzkes, D.R.},  Journal = {Clinical Infectious Diseases},  Pages = {236--242},  Title = {Antiviral activity of lamivudine in salvage therapy for multidrug-resistant HIV-1 infection},  Volume = {41},  Year = {2005}}  @article{Cao1994,  Author = {Cao, Y. and Adachi, J. and Yano, T. and Hasegawa, M.},  Journal = {Molecular Biology and Evolution},  Pages = {593--604},  Title = {Phylogenetic place of guinea pigs: no support of the rodent-polyphyly hypothesis from maximum-likelihood analyses of multiple protein sequences},  Volume = {11},  Year = {1994}}  @article{Cao1998,  Author = {Cao, Y. and Janke, A. and Waddell, P.J. and Westerman, M. and Takenaka, O. and Murata, S. and Okada, N. and Paabo, S. and Hasegawa, M.},  Journal = {Journal of Molecular Evolution},  Pages = {307--322},  Title = {Conflict among individual mitochondrial proteins in resolving the phylogeny of Eutherian orders},  Volume = {47},  Year = {1998}}  @article{Cao1997,  Author = {Cao, Y. and Okada, N. and Hasegawa, M.},  Journal = {Molecular Biology and Evolution},  Pages = {461--464},  Title = {Phylogenetic position of guinea-pigs revisited},  Volume = {14},  Year = {1997}}  @article{Carlin1995,  Author = {Carlin, B.P. and Chib, S.},  Journal = {Journal of the Royal Statistical Society, Series B},  Pages = {473--484},  Title = {Bayesian model choice via Markov chain Monte Carlo methods},  Volume = {57},  Year = {1995}}  @article{Carpenter1995,  Author = {Carpenter, C.D. and Oh, J.W. and Zang, C. and Simon, A.E.},  Journal = {Journal of Molecular Biology},  Pages = {608--622},  Title = {Involvement of a stem-loop structure in the location of junction sites in viral RNA recombination},  Volume = {245},  Year = {1995}}  @article{Cascone1993,  Author = {Cascone, P.J. and Haydar, T.F. and Simon, A.E.},  Journal = {Science},  Pages = {801--805},  Title = {Sequences and structures required for recombination between virus-associated RNAs},  Volume = {260},  Year = {1993}}  @article{Casella1998,  Author = {Casella, G. and Robert, C.P.},  Journal = {Journal of Computational and Graphical Statistics},  Pages = {139--157},  Title = {Post-processing accept-reject samples: recycling and rescaling},  Volume = {7},  Year = {1998}}  @article{Casella1998a,  Author = {Casella, G. and Robert, C.P.},  Journal = {Journal of Computational and Graphical Statistics},  Pages = {139--157},  Title = {Post-processing accept-reject samples: Recycling the rescaling},  Volume = {7},  Year = {1998}}  @article{Casella1996,  Author = {Casella, G. and Robert, C.P.},  Journal = {Biometrika},  Pages = {81--94},  Title = {Rao-Blackwellisation of sampling schemes},  Volume = {83},  Year = {1996}}  @techreport{Casella2000,  Author = {Casella, G. and Robert, C.P. and Wells, M.T.},  Title = {Mixture models, latent variables and partitioned importance sampling},  Year = {2000}}  @article{Cavalli-Sforza1967,  Author = {Cavalli-Sforza, L.L. and Edwards, A.W.F.},  Journal = {American Journal of Human Genetics},  Pages = {233--257},  Title = {Phylogenetic analysis: models and estimation procedures},  Volume = {19},  Year = {1967}}  @article{Champagnat2007,  Author = {Champagnat, Nicolas and Lambert, Amaury},  Date-Added = {2008-03-28 15:45:14 +1300},  Date-Modified = {2008-03-28 15:45:17 +1300},  Doi = {DOI 10.1214/105051606000000628},  Journal = {Annals of Applied Probability},  Keywords = {logistic branching process; 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Editor = {Du, D.Z. and Pardalos, P.M. and Wang, J.},  Pages = {35--76},  Publisher = {Kluwer Academic Publishers},  Title = {On computing the nearest neighbor interchange distance},  Year = {1999}}  @article{DasGupta1997,  Author = {DasGupta, B. and He, X. and Jiang, T. and Li, M. and Tromp, J. and Zhang, L.},  Journal = {Proceedings of the 8th ACM-SIAM Symposium on Discrete Algorithms},  Pages = {427--436},  Title = {On distances between phylogenetics trees},  Year = {1997}}  @article{Daubin2003,  Author = {Daubin, V. and Moran, N.A. and Ochman, H.},  Journal = {Science},  Notes = {HGT},  Pages = {829--832},  Title = {Phylogenetics and the cohesion of bacterial genomes},  Volume = {301},  Year = {2003}}  @article{Davidian1993,  Author = {Davidian, M. and Gallant, A.R.},  Journal = {Biometrika},  Pages = {475--488},  Title = {The nonlinear mixed effects model with a smooth random effects density},  Volume = {80},  Year = {1993}}  @article{Davidian1993a,  Author = {Davidian, M. and Giltinan, D.M.},  Journal = {Biometrics},  Pages = {59--73},  Title = {Some simple methods for estimating intraindividual variability in nonlinear mixed effects models},  Volume = {49},  Year = {1993}}  @article{Davis1997,  Author = {Davis, S. and Weeks, D.E.},  Journal = {American Journal of Human Genetics},  Pages = {1431--1444},  Title = {Comparison of nonparametric statistics for detection of linkage in nuclear families: Single-marker evaluation},  Volume = {61},  Year = {1997}}  @article{Deckert1998,  Author = {Deckert, G. and Warren, P.V. and Gaasterland, T. and Young, W.G. and Lenox, A.L. and Graham, D.E. and Overbeek, R. and Snead, M.A. and Keller, M. and Aujay, M. and Huber, R. and Feldman, R.A. and Short, J.M. and Olsen, G.J. and Swanson, R.V.},  Journal = {Nature},  Pages = {353--358},  Title = {The complete genome of the hyperthermophilic bacterium Aquifex aeoclicus},  Volume = {392},  Year = {1998}}  @article{Deeks2003,  Author = {Deeks, S.G. and Grant, R.M. and Wrin, T. and Paxinos, E.E. and Liegler, T. and Hoh, R. and Martin, J.N. and Petropoulos, C.J.},  Journal = {AIDS},  Pages = {361--370},  Title = {Persistence of drug-resistant HIV-1 after a structured treatment interruption and its impact on treatment response},  Volume = {17},  Year = {2003}}  @article{Deeks2005,  Author = {Deeks, S.G. and Hoh, R. and Neilands, T.B. and Liegler, T. and Aweeka, F. and Petropoulos, C.J. and Grant, R.M. and Martin, J.N.},  Journal = {Journal of Infectious Diseases},  Pages = {1537--1544},  Title = {Interruption of treatment with individual therapeautic drug classes in adults with multidrug-resistant HIV-1 infection},  Volume = {192},  Year = {2005}}  @article{Dellaportas1999,  Author = {Dellaportas, P. and Forster, J.J.},  Journal = {Biometrika},  Notes = {DAG; model selection},  Pages = {615--633},  Title = {Markov chain Monte Carlo model determination for hierarchical and graphical log-linear models},  Volume = {86},  Year = {1999}}  @article{Dellaportas2002,  Author = {Dellaportas, P. and Forster, J.J. and Ntzoufras, I.},  Journal = {Statistics and Computing},  Notes = {model selection},  Pages = {27--36},  Title = {On Bayesian model and variable selection using MCMC},  Volume = {12},  Year = {2002}}  @article{Dellaportas1993,  Author = {Dellaportas, P. and Smith, A.F.M.},  Journal = {Applied Statistics},  Pages = {443--459},  Title = {Bayesian inference for generalized linear and proportional hazards models via Gibbs sampling},  Volume = {42},  Year = {1993}}  @article{Dempster1950,  Author = {Dempster, E.R. and Lerner, I.M.},  Journal = {Genetics},  Pages = {212--236},  Title = {Heritability of threshold characters},  Volume = {35},  Year = {1950}}  @article{Deng1996,  Author = {Deng, H. and Liu, R. and Ellmeier, W. and Choe, S. and Unutmaz, D. and Burkhart, M. and Marzio, P. Di and Marmon, S. and Sutton, R.E. and Hill, C.M. and Davis, C.B. and Peiper, S.C. and Schall, T.J. and Littman, D.R. and Landau, N.R.},  Journal = {Nature},  Pages = {661--666},  Title = {Identification of a major coreceptor for primary isolates for HIV-1},  Volume = {381},  Year = {1996}}  @book{Denison2002,  Address = {New York, NY},  Author = {Denison, D. G. T. and Holmes, C. C. and Mallick, B. K. and Smith, A. F. M.},  Date-Modified = {2014-07-06 03:59:51 +0000},  Publisher = {John Wiley \& Sons},  Title = {Bayesian Methods for Nonlinear Classification and Regression},  Year = {2002}}  @article{Denison1998,  Author = {Denison, D.G.T. and Mallick, B.K. and Smith, A.F.M},  Journal = {Journal of the Royal Statistical Society, Series B},  Pages = {333--350},  Title = {Automatic Bayesian curve fitting},  Volume = {60},  Year = {1998}}  @article{DeRisi1997,  Author = {DeRisi, J.L. and Iyer, V.R. and Brown, P.O.},  Journal = {Science},  Notes = {yeast expression},  Pages = {680--686},  Title = {Exploring the metabolic and genetic control of gene expression on a genomic scale},  Volume = {278},  Year = {1997}}  @article{Desharnais2006,  Abstract = {A scaling rule of ecological theory, accepted but lacking experimental  confirmation, is that the magnitude of fluctuations in population  densities due to demographic stochasticity scales inversely with  the square root of population numbers. This supposition is based  on analyses of models exhibiting exponential growth or stable equilibria.  Using two quantitative measures, we extend the scaling rule to situations  in which population densities fluctuate due to nonlinear deterministic  dynamics. These measures are applied to populations of the flour  beetle Tribolium castaneum that display chaotic dynamics in both  20-g and 60-g habitats. Populations cultured in the larger habitat  exhibit a clarification of the deterministic dynamics, which follows  the inverse square root rule. Lattice effects, a deterministic phenomenon  caused by the discrete nature of individuals, can cause deviations  from the scaling rule when population numbers are small. The scaling  rule is robust to the probability distribution used to model demographic  variation among individuals.},  Au = {Desharnais, RA and Costantino, RF and Cushing, JM and Henson, SM and Dennis, B and King, AA},  Author = {Desharnais, Robert A and Costantino, R F and Cushing, J M and Henson, Shandelle M and Dennis, Brian and King, Aaron A},  Da = {20060428},  Date-Added = {2008-04-13 17:20:00 +1200},  Date-Modified = {2008-04-13 17:30:27 +1200},  Dcom = {20060508},  Doi = {10.1111/j.1461-0248.2006.00903.x},  Edat = {2006/04/29 09:00},  Issn = {1461-0248 (Electronic)},  Jid = {101121949},  Journal = {Ecol Lett},  Jt = {Ecology letters},  Language = {eng},  Lr = {20061115},  Mh = {Animals; Demography; Environment; Female; Male; *Models, Theoretical; Population Density; Population Dynamics; Tribolium/*growth \& development},  Mhda = {2006/05/09 09:00},  Number = {5},  Own = {NLM},  Pages = {537--547},  Pii = {ELE903},  Pl = {England},  Pmid = {16643299},  Pst = {ppublish},  Pt = {Letter; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Ecol Lett. 2006 May;9(5):537-47.},  Stat = {MEDLINE},  Title = {Experimental support of the scaling rule for demographic stochasticity.},  Volume = {9},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1461-0248.2006.00903.x}}  @article{Detels1998,  Author = {Detels, R. and Munoz, A. and McFarlane, G. and Kingsley, L.A. and Margolick, J.B. and Giorgi, J. and Schrager, L.K. and Phair, J.P.},  Journal = {Journal of the American Medical Association},  Pages = {1497--1503},  Title = {Effectiveness of potent antiretroviral therapy on time to AIDS and death in men with known HIV infection duration. Multicenter AIDS Cohort Study Investigators},  Volume = {280},  Year = {1998}}  @article{Deuar2001,  Author = {Deuar, P. and Drummond, P. D.},  Date-Added = {2008-04-12 21:27:27 +1200},  Date-Modified = {2014-07-06 00:48:51 +0000},  Journal = {Computer Physics Communications},  Pages = {442-445},  Title = {Stochastic gauges in quantum dynamics for many-body simulations},  Volume = {142},  Year = {2001}}  @article{Devine2002,  Author = {Devine, C. and Hinman, V.F. and Degnan, B.M.},  Journal = {International Journal of Developmental Biology},  Notes = {Expression},  Pages = {687--692},  Title = {Evolution and developmental expression of nuclear receptor genes in the ascidian Herdmania},  Volume = {46},  Year = {2002}}  @article{Dickey1971,  Author = {Dickey, J.M.},  Journal = {The Annals of Mathematical Statistics},  Pages = {204--223},  Title = {The weighted likelihood ratio, linear hypotheses on normal location parameters},  Volume = {42},  Year = {1971}}  @article{Dickey1970,  Author = {Dickey, J.M. and Lientz, B.P.},  Journal = {The Annals of Mathematical Statistics},  Pages = {214--226},  Title = {The weighted likelihood ratio, sharp hypotheses about chances, the order of a Markov chain},  Volume = {41},  Year = {1970}}  @article{Diebolt1994,  Author = {Diebolt, J. and Robert, C.},  Journal = {Journal of the Royal Statistical Society, Series B},  Pages = {363--375},  Title = {Estimation of finite mixture distributions through Bayesian sampling},  Volume = {56},  Year = {1994}}  @article{Diggle1984,  Author = {Diggle, P.J. and Gratton, R.J.},  Journal = {Journal of Royal Statistical Society, B},  Pages = {193--227},  Title = {Monte Carlo methods of inference for implicit statistical models},  Volume = {46},  Year = {1984}}  @article{DiMatteo2001,  Author = {DiMatteo, I. and Genovese, C.R. and Kass, R.E.},  Journal = {Biometrika},  Notes = {reversible jump MCMC},  Pages = {1055--1071},  Title = {Bayesian curve fitting with free-knot splines},  Volume = {88},  Year = {2001}}  @techreport{DiMatteo2000,  Author = {DiMatteo, I. and Genovese, C.R. and Kass, R.E.},  Institution = {Department of Statistics, Carnegie Mellon University},  Number = {716},  Title = {Bayesian curve fitting with free-knot splines},  Year = {2000}}  @book{Dobbins1987,  Address = {Springfield, IL},  Author = {Dobbins, W.O.},  Publisher = {Thomas},  Title = {Whipple's Disease},  Year = {1987}}  @article{Doering2005,  Author = {Doering, C.R. and Sargsyan, K.V. and Sanders, L.M.},  Date-Added = {2008-03-28 16:31:18 +1300},  Date-Modified = {2008-03-28 16:32:27 +1300},  Journal = {SIAM Journal of Multiscale Modeling and simulation},  Pages = {283-299},  Title = {Extinction times for birth-death processes: exact results, continuum asymptotics, and the failure of the Fokker-Planck approximation},  Volume = {3},  Year = {2005}}  @article{Dong2001,  Author = {Dong, W.L. and Caldeira, S. and Sehr, P. and Pawlita, M. and Tommasino, M.},  Journal = {Journal of Virological Methods},  Notes = {HPV},  Pages = {91--98},  Title = {Determination of the binding affinity of different human papillomavirus E7 proteins for the tumor suppressor prb by a plate-binding assay},  Volume = {98},  Year = {2001}}  @article{Donnelly1999,  Author = {Donnelly, P. and Kurtz, T.G.},  Journal = {Annals of Applied Probability},  Pages = {1091--1148},  Title = {Genealogical processes for Fleming-Viot models with selections and recombination},  Volume = {9},  Year = {1999}}  @article{Doolittle2000,  Author = {Doolittle, W.F.},  Journal = {Scientific American},  Notes = {HGT},  Pages = {90--95},  Title = {Uprooting the tree of life},  Volume = {February},  Year = {2000}}  @article{Doolittle1999,  Author = {Doolittle, W.F.},  Journal = {Science},  Notes = {HGT},  Pages = {1443a},  Title = {Lateral gene transfer, genome surveys and the phylogeny of prokaryotes [technical comments]},  Volume = {286},  Year = {1999}}  @article{Doolittle1999a,  Author = {Doolittle, W.F.},  Journal = {Science},  Notes = {HGT},  Pages = {2124--2128},  Title = {Phylogenetic classification and the universal tree},  Volume = {284},  Year = {1999}}  @article{Dorman2001,  Author = {Dorman, K.S. and Kaplan, A.H. and Lange, K. and Sinsheimer, J.S.},  Journal = {Journal of Acquired Immune Deficiency Symdromes},  Pages = {398--402},  Title = {Mutation takes no vacation: can structed treatment interruptions increase the risk of drug-resistant HIV-1?},  Volume = {25},  Year = {2001}}  @article{Dorman2002,  Author = {Dorman, K.S. and Kaplan, A.H. and Sinsheimer, J.S.},  Journal = {Journal of Molecular Evolution},  Pages = {200--209},  Title = {Bootstrap confidence levels for HIV-1 recombination},  Volume = {54},  Year = {2002}}  @article{Dorman2004,  Author = {Dorman, K.S. and Sinsheimer, J.S. and Lange, K.},  Journal = {SIAM Review},  Pages = {202--229},  Title = {In the garden of branching processes},  Volume = {46},  Year = {2004}}  @article{Douzery2003,  Author = {Douzery, E.J.P. and Delsuc, P. and Stanhope, M.J. and Huchon, D.},  Journal = {Journal of Molecular Evolution},  Pages = {S201-S213},  Title = {Local molecular clocks in three nuclear genes: divergence times for rodents and other mammals and incompatibility among fossil calibrations},  Volume = {57},  Year = {2003}}  @article{Dowson1989,  Author = {Dowson, C.G. and Hutchison, A. and Brannigan, J.A. and George, R.C. and Hansman, D. and Linares, J. and Tomasz, A. and Smith, J. Maynard and Spratt, B.G.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {8842-8846},  Title = {Horizontal transfer of penicillin-binding protein genes in penicillin-resistant clinical isolates of Streptococcus pneumoniae},  Volume = {86},  Year = {1989}}  @article{Doyle1992,  Author = {Doyle, J.J.},  Journal = {Systematic Botany},  Notes = {incongruence},  Pages = {144--163},  Title = {Gene trees and species trees: molecular systematics as one-character taxonomy},  Volume = {17},  Year = {1992}}  @article{Drake2006,  Abstract = {Predicting population extinctions is a key element of quantitative  conservation biology and population ecology. Although stochastic  population theories have long been used to obtain theoretical distributions  of population extinction times, model-based predictions have rarely  been tested. Here I report results from a quantitative analysis of  extinction time in 281 experimental populations of water fleas (Daphnia  magna) in variable environments. To my knowledge, this is the first  quantitative estimate of the shape of the distribution of population  extinction times based on extinction data for any species. The finding  that the distribution of population extinction times was extraordinarily  peaked is consistent with theoretical predictions for density-independent  populations, but inconsistent with predictions for density-dependent  populations. The tail of the extinction time distribution was not  exponential. These results imply that our current theories of extinction  are inadequate. Future work should focus on how demographic stochasticity  scales with population size and effects of nonrandom variable environments  on population growth and decline.},  Address = {National Center for Ecological Analysis and Synthesis, 735 State Street, Ste. 300, Santa Barbara, California 93101, USA. [email protected]},  Au = {Drake, JM},  Author = {Drake, John M},  Da = {20060925},  Date-Added = {2008-04-13 17:20:00 +1200},  Date-Modified = {2008-04-13 17:27:45 +1200},  Edat = {2006/09/26 09:00},  Issn = {0012-9658 (Print)},  Jid = {0043541},  Journal = {Ecology},  Jt = {Ecology},  Language = {eng},  Mhda = {2006/09/26 09:00},  Number = {9},  Own = {NLM},  Pages = {2215--2220},  Pl = {United States},  Pmid = {16995621},  Pst = {ppublish},  Pt = {Comparative Study; Journal article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Ecology. 2006 Sep;87(9):2215-20.},  Stat = {In-Process},  Title = {Extinction times in experimental populations.},  Volume = {87},  Year = {2006}}  @article{Drummond2001,  Author = {Drummond, A. J. and Forsberg, R. and Rodrigo, A. G.},  Date-Modified = {2014-07-06 01:00:40 +0000},  Journal = {Molecular Biology and Evolution},  Notes = {serial},  Pages = {1365--1371},  Title = {The inference of stepwise changes in substitution rates using serial sequence samples},  Volume = {18},  Year = {2001}}  @article{Drummond2003,  Author = {Drummond, A. J. and Pybus, O. G. and Rambaut, A. and Forsberg, R. and Rodrigo, A. G.},  Date-Modified = {2014-07-06 00:50:13 +0000},  Journal = {Trends in Ecology \& Evolution},  Pages = {481--488},  Title = {Measurably evolving populations},  Volume = {18},  Year = {2003}}  @article{Drummond2000,  Author = {Drummond, A. J. and Rodrigo, A. G.},  Date-Modified = {2014-07-06 00:49:07 +0000},  Journal = {Molecular Biology and Evolution},  Notes = {serial},  Number = {12},  Pages = {1807--1815},  Title = {Reconstructing genealogies of serial samples under the assumption of a molecular clock using serial-sample UPGMA},  Volume = {17},  Year = {2000}}  @article{Drummond2004,  Author = {Drummond, P. D.},  Date-Added = {2008-04-12 21:34:38 +1200},  Date-Modified = {2014-07-06 00:51:05 +0000},  Journal = {European Physical Journal B},  Number = {4},  Pages = {617-634},  Title = {Gauge Poisson representations for birth/death master equations},  Volume = {38},  Year = {2004}}  @article{Drummond2003a,  Author = {Drummond, P. D. and Deuar, P.},  Date-Added = {2008-04-12 21:30:37 +1200},  Date-Modified = {2014-07-06 00:49:19 +0000},  Journal = {Journal of Optics B: Quantum and Semiclassical Optics},  Pages = {S281-S289},  Title = {Quantum dynamics with stochastic gauge simulations},  Volume = {5},  Year = {2003}}  @article{Dudoit2002,  Author = {Dudoit, S. and Fridlyand, F. and Speed, T.P.},  Journal = {Journal of the American Statistical Association},  Pages = {77--87},  Title = {Comparison of discrimination methods for the classification of tumors using gene expression data},  Volume = {97},  Year = {2002}}  @book{Durbin1998,  Address = {Cambridge},  Author = {Durbin, R. and Eddy, S. and Krogh, A. and Mitchinson, G.},  Publisher = {Cambridge University Press},  Title = {Biological Sequence Analysis: Probabilistic Models of Proteins and Nucleic Acids},  Year = {1998}}  @article{Dushoff2000,  Abstract = {The stochastic logistic model is the simplest model that combines  individual-level demography with density dependence. It explicitly  or implicitly underlies many models of biodiversity of competing  species, as well as non-spatial or metapopulation models of persistence  of individual species. The model has also been used to study persistence  in simple disease models. The stochastic logistic model has direct  relevance for questions of limiting similarity in ecological systems.  This paper uses a biased random walk heuristic to derive a scaling  relationship for the persistence of a population under this model,  and discusses its implications for models of biodiversity and persistence.  Time to extinction of a species under the stochastic logistic model  is approximated by the exponential of the scaling quantity U=(R-1)(2)  N/R(R+1), where N is the habitat size and R is the basic reproductive  number.},  Address = {Institute of Physics, Academia Sinica, Nankang 105, Taipei, Taiwan.},  Au = {Dushoff, J},  Author = {Dushoff, J},  Ci = {Copyright 2000 Academic Press.},  Da = {20000413},  Date-Added = {2008-03-28 15:30:44 +1300},  Date-Modified = {2008-03-28 15:42:35 +1300},  Dcom = {20000413},  Doi = {10.1006/tpbi.1999.1434},  Edat = {2000/03/10 09:00},  Issn = {0040-5809 (Print)},  Jid = {0256422},  Journal = {Theor Popul Biol},  Jt = {Theoretical population biology},  Keywords = {stochastic logistic},  Language = {eng},  Lr = {20031114},  Mh = {Animals; Bias (Epidemiology); Competitive Behavior/*physiology; *Demography; *Ecosystem; Finite Element Analysis; *Logistic Models; *Population Density; Reproduction; Selection (Genetics); Species Specificity; *Stochastic Processes; Time Factors},  Mhda = {2000/04/15 09:00},  Number = {1},  Own = {NLM},  Pages = {59--65},  Pii = {S0040-5809(99)91434-X},  Pl = {UNITED STATES},  Pmid = {10708629},  Pst = {ppublish},  Pt = {Journal article},  Pubm = {Print},  Sb = {IM},  So = {Theor Popul Biol. 2000 Feb;57(1):59-65.},  Stat = {MEDLINE},  Title = {Carrying capacity and demographic stochasticity: scaling behavior of the stochastic logistic model.},  Volume = {57},  Year = {2000},  Bdsk-Url-1 = {http://dx.doi.org/10.1006/tpbi.1999.1434}}  @article{Dyk,  Author = {Dyk, D.A. Van and Meng, X.-L.},  Journal = {Journal of Computational and Graphical Statistics},  Pages = {1--50},  Title = {The art of data augmentation},  Volume = {10}}  @article{Editor-Nature1999,  Author = {Sen-Editor-Nature},  Journal = {Nature},  Pages = {843},  Title = {Combating the exploiters of creationism},  Volume = {402},  Year = {1999}}  @article{Edwards1970,  Author = {Edwards, A.W.F.},  Journal = {Journal of the Royal Statistical Society, Series B},  Notes = {tree shape},  Pages = {155--174},  Title = {Estimation of the branch points of a branching diffusion process (with discussion)},  Volume = {32},  Year = {1970}}  @article{Efron1996,  Author = {Efron, B. and Halloran, E. and Holmes, S.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {13429--13434},  Title = {Bootstrap confidence levels for phylogenetic trees},  Volume = {93},  Year = {1996}}  @article{Efron2002,  Author = {Efron, B. and Tibshirani, R.},  Journal = {Genetic Epidemiology},  Notes = {FDR},  Pages = {70-86},  Title = {Empirical Bayes methods and false discovery rates for microarrays},  Volume = {23},  Year = {2002}}  @book{Efron1993,  Address = {New York},  Author = {Efron, B. and Tibshirani, R.J.},  Publisher = {Chapman \& Hall},  Series = {Monographs on Statistics and Applied Probability 57},  Title = {An Introduction to the Bootstrap},  Year = {1993}}  @incollection{Efroymson1960,  Address = {New York},  Author = {Efroymson, M.A.},  Booktitle = {Mathematical Methods for Digital Computers},  Editor = {Ralston, A. and Wilf, H.S.},  Pages = {191--203},  Publisher = {Wiley},  Title = {Multiple regression analysis},  Year = {1960}}  @article{Eilers1996,  Author = {Eilers, P.H.C. and Marx, B.D.},  Journal = {Statistical Science},  Notes = {splines},  Pages = {89--121},  Title = {Flexible smoothing with B-splines and penalties},  Volume = {11},  Year = {1996}}  @article{Eisen1998,  Author = {Eisen, M.B. and Spellman, P.T. and Brown, P.O. and Botstein, D.},  Journal = {Proceedings of the National Academies of Science, USA},  Notes = {yeast expression},  Pages = {14863--14868},  Title = {Cluster analysis and display of genome-wide expression patterns},  Volume = {95},  Year = {1998}}  @conference{El-Sadr2006,  Address = {,\ Denver, CO},  Author = {El-Sadr, W. and Neaton, J. and Team, SMART Study},  Booktitle = {13th Conference on Retroviruses and Opportunistic Infections},  Month = {February},  Title = {Strategies for management of antiretroviral therapy study},  Year = {2006}}  @article{Engen2007,  Abstract = {We derive formulas that can be applied to estimate the effective population  size N(e) for organisms with two sexes reproducing once a year and  having constant adult mean vital rates independent of age. Temporal  fluctuations in population size are generated by demographic and  environmental stochasticity. For populations with even sex ratio  at birth, no deterministic population growth and identical mean vital  rates for both sexes, the key parameter determining N(e) is simply  the mean value of the demographic variance for males and females  considered separately. In this case Crow and Kimura's generalization  of Wright's formula for N(e) with two sexes, in terms of the effective  population sizes for each sex, is applicable even for fluctuating  populations with different stochasticity in vital rates for males  and females. If the mean vital rates are different for the sexes  then a simple linear combination of the demographic variances determines  N(e), further extending Wright's formula. For long-lived species  an expression is derived for N(e) involving the generation times  for both sexes. In the general case with nonzero population growth  and uneven sex ratio of newborns, we use the model to investigate  numerically the effects of different population parameters on N(e).  We also estimate the ratio of effective to actual population size  in six populations of house sparrows on islands off the coast of  northern Norway. This ratio showed large interisland variation because  of demographic differences among the populations. Finally, we calculate  how N(e) in a growing house sparrow population will change over time.},  Address = {Population Biology Center, Department of Mathematical Sciences, Norwegian University of Science and Technology, N-7491 Trondheim, Norway. [email protected]},  Au = {Engen, S and Ringsby, TH and Saether, BE and Lande, R and Jensen, H and Lillegard, M and Ellegren, H},  Author = {Engen, Steinar and Ringsby, Thor Harald and Saether, Bernt-Erik and Lande, Russell and Jensen, Henrik and Lillegard, Magnar and Ellegren, Hans},  Da = {20070808},  Date-Added = {2008-04-13 17:20:00 +1200},  Date-Modified = {2008-04-13 17:22:21 +1200},  Dcom = {20071108},  Doi = {10.1111/j.1558-5646.2007.00155.x},  Edat = {2007/08/09 09:00},  Issn = {0014-3820 (Print)},  Jid = {0373224},  Journal = {Evolution Int J Org Evolution},  Jt = {Evolution; international journal of organic evolution},  Language = {eng},  Mh = {Animals; Female; Male; *Models, Biological; Population Density; Population Dynamics; *Reproduction; Sex Factors; *Sparrows; Time Factors},  Mhda = {2007/11/09 09:00},  Number = {8},  Own = {NLM},  Pages = {1873--1885},  Pii = {EVO155},  Pl = {United States},  Pmid = {17683430},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Validation Studies},  Pubm = {Print},  Sb = {IM},  So = {Evolution Int J Org Evolution. 2007 Aug;61(8):1873-85.},  Stat = {MEDLINE},  Title = {Effective size of fluctuating populations with two sexes and overlapping generations.},  Volume = {61},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1558-5646.2007.00155.x}}  @article{Engen2000,  Abstract = {Populations threatened by extinction are often far below their carrying  capacity. A population collapse or quasi-extinction is defined to  occur when the population size reaches some given lower density.  If this density is chosen to be large enough for the demographic  stochasticity to be ignored compared to environmental stochasticity,  then the logarithm of the population size may be modelled by a Brownian  motion until quasi-extinction occurs. The normal-gamma mixture of  inverse Gaussian distributions can then be applied to define prediction  intervals for the time to quasi-extinction in such processes. A similar  mixture is used to predict the population size at a finite time for  the same process provided that quasi-extinction has not occurred  before that time. Stochastic simulations indicate that the coverage  of the prediction interval is very close to the probability calculated  theoretically. As an illustration, the method is applied to predict  the time to extinction of a declining population of white stork in  southwestern Germany.},  Address = {Department of Mathematical Sciences, Norwegian University of Science and Technology, Trondheim, N-7491, Norway.},  Au = {Engen, S and Saether, BE},  Author = {Engen, S and Saether, B E},  Ci = {Copyright 2000 Academic Press.},  Da = {20000914},  Date-Added = {2008-04-13 17:32:20 +1200},  Date-Modified = {2008-04-13 17:38:07 +1200},  Dcom = {20000914},  Doi = {10.1006/jtbi.2000.2094},  Edat = {2000/08/10 11:00},  Issn = {0022-5193 (Print)},  Jid = {0376342},  Journal = {J Theor Biol},  Jt = {Journal of theoretical biology},  Language = {eng},  Lr = {20061115},  Mh = {Animals; *Birds; *Models, Statistical; *Population Dynamics; Time Factors},  Mhda = {2000/09/19 11:01},  Number = {4},  Own = {NLM},  Pages = {649--658},  Pii = {S0022-5193(00)92094-0},  Pl = {ENGLAND},  Pmid = {10931759},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Sb = {IM},  So = {J Theor Biol. 2000 Aug 21;205(4):649-58.},  Stat = {MEDLINE},  Title = {Predicting the time to quasi-extinction for populations far below their carrying capacity.},  Volume = {205},  Year = {2000},  Bdsk-Url-1 = {http://dx.doi.org/10.1006/jtbi.2000.2094}}  @article{Equils2000,  Author = {Equils, O. and Garratty, E. and Wei, L.S. and Plaeger, S. and Tapia, M. and Deville, J. and Krogstad, P. and Sim, M-S and Nielksen, K. and Bryson, Y.},  Journal = {Journal of Infectious Diseases},  Pages = {751--7},  Title = {Recovery of replication-competent virus from CD4 T cell reservoirs and change in coreceptor use in HIV-1 infected children responding to HAART.},  Volume = {182},  Year = {2000}}  @article{Eron2004,  Author = {Eron, J.J. and Barlett, J.A. and Santana, J.L. and Bellos, N.C. and Johnson, J. and Keller, A. and Kuritzkes, D.R. and St.~Clair, M.H. and Johnson, V.A.},  Journal = {Journal of Acquired Immune Deficiency Syndromes},  Pages = {1581--1583},  Title = {Persistent antiretroviral activity of nucleoside analogues after prolonged zidovudine and lamivudine therapy as demonstrated by rapid loss of activity after discontinuation},  Volume = {37},  Year = {2004}}  @article{Escobar1995,  Author = {Escobar, M.D. and West, M.},  Journal = {Journal of the American Statistical Assocation},  Notes = {mixture},  Pages = {577-588},  Title = {Bayesian density estimation and inference using mixtures},  Volume = {90},  Year = {1995}}  @article{Este1999,  Author = {Este, J.A. and Cabrera, C. and Blanco, J. and Gutierrez, A. and Bridger, G. and Henson, G. and Schols, D. and DeClercq, E.},  Journal = {Journal of Virology},  Pages = {5577--5585},  Title = {Shift of clinical human immunodeficiency virus type 1 isolates from X4 to R5 and prevention of emergence of the syncytium-inducing phenotype by blockade of CXCR4},  Volume = {73},  Year = {1999}}  @book{Eubank1999,  Address = {New York, NY},  Author = {Eubank, R.L.},  Publisher = {Marcel Dekker, Inc.},  Title = {Nonparametric Regression and Spline Smoothing},  Year = {1999}}  @article{Eyre-Walker1999,  Author = {Eyre-Walker, A. and Smith, N.H. and Smith, J.M.},  Journal = {Proceedings of the Royal Society of London, B},  Pages = {477--483},  Title = {How clonal are human mitochondria?},  Volume = {266},  Year = {1999}}  @article{Fang2004,  Author = {Fang, G. and Weiser, B. and Kuiken, C. and Phipott, S.M. and Rowland-Jones, S. and Plummer, F. and Kimani, J. and Shi, B. and Kaul, R. and Bwayo, J. and Anzala, O. and Burger, H.},  Journal = {AIDS},  Pages = {153--159},  Title = {Recombination following superinfection by HIV-1},  Volume = {18},  Year = {2004}}  @article{Fang1998,  Author = {Fang, G. and Zhu, G. and Burger, H. and Keithly, J. and Weiser, B.},  Journal = {Journal of Virology Methods},  Pages = {139--148},  Title = {Minimizing DNA recombination during long RT-PCR},  Volume = {76},  Year = {1998}}  @article{Farci2000,  Author = {Farci, P. and Shimoda, A. and Coiana, A. and Diaz, G. and Peddis, G. and Melpolder, J.C. and Strazzera, A. and Chien, D.Y. and Munoz, S.J. and Balestrieri, A. and Purcell, R.H. and Alter, H.J.},  Journal = {Science},  Notes = {beta-prior},  Number = {5464},  Pages = {339--344},  Title = {The outcome of acute hepatitis C predicted by the evolution of the viral quasispecies},  Volume = {288},  Year = {2000}}  @article{Farci2002,  Author = {Farci, P. and Strazzera, R. and Alter, H.J. and Farci, S. and Degioannis, D. and Coiana, A. and Peddis, G. and Usai, F. and Serra, G. and Diaz, G. and Balestrieri, A. and Purcell, R.H.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {3081--3086},  Title = {Early changes in hepatitis C viral quasispecies during interferon therapy predict the therapeutic outcome},  Volume = {99},  Year = {2002}}  @article{fearnhead2001,  Author = {Fearnhead, P. and Donnelly, P.},  Journal = {Genetics},  Number = {3},  Pages = {1299},  Publisher = {Genetics Soc America},  Title = {{Estimating recombination rates from population genetic data}},  Volume = {159},  Year = {2001}}  @book{Feller1971,  Address = {New York},  Author = {Feller, W.},  Edition = {2nd},  Publisher = {John Wiley \& Sons},  Title = {An Introduction to Probability Theory and Its Applications, Vol. II},  Year = {1971}}  @book{Feller1968,  Author = {Feller, W.},  Edition = {3rd},  Location = {New York, NY},  Publisher = {John Wiley \& Sons, Inc.},  Title = {An Introduction to Probability Theory and Its Applications, Volume 1},  Year = {1968}}  @book{Feller1968a,  Address = {New York},  Author = {Feller, W.},  Edition = {3rd},  Publisher = {John Wiley and Sons},  Title = {An Introduction to Probability Theory and Its Applications, Vol. II},  Year = {1968}}  @inproceedings{Feller1951,  Address = {Berkeley},  Author = {Feller, W.},  Booktitle = {Proc. Second Berkeley Symp. Math. Statist. Probab.},  Date-Added = {2008-03-28 16:44:30 +1300},  Date-Modified = {2008-03-28 16:46:12 +1300},  Pages = {227-246},  Publisher = {Univ. California Press},  Title = {Diffusion processes in genetics},  Year = {1951}}  @article{Feller1939,  Author = {Feller, W.},  Date-Added = {2008-03-28 16:21:11 +1300},  Date-Modified = {2008-03-28 16:22:07 +1300},  Journal = {Acta Biotheor.},  Pages = {11-40},  Title = {Die Grundlagen der Volterraschen Theorie des Kampfes ums Dasein in wahrscheinlichkeitstheoretiseher Be.handlung},  Volume = {5},  Year = {1939}}  @article{Felsenstein2005,  Author = {Felsenstein, J.},  Journal = {Philosophical Transactions of the Royal Society of London, Series B},  Pages = {1427--1434},  Title = {Using the quantitative genetic threshold model for inferences between and within species},  Volume = {360},  Year = {2005}}  @book{Felsenstein2004,  Address = {Sunderland, MA},  Author = {Felsenstein, J.},  Publisher = {Sinauer Associates, Inc.},  Title = {Inferring Phylogenies},  Year = {2004}}  @book{Felsenstein1993,  Address = {Seattle, WA},  Author = {Felsenstein, J.},  Publisher = {Distributed by the author. Department of Genetics, University of Washington},  Title = {PHYLIP (Phylogenetic Inference Package), Version 3.5},  Year = {1993}}  @article{Felsenstein1992,  Author = {Felsenstein, J.},  Journal = {Genetical Research},  Pages = {139--147},  Title = {Estimating effective population size from samples of sequences: inefficiency of pairwise and segregating sites as compared to phylogenetic estimates},  Volume = {59},  Year = {1992}}  @article{Felsenstein1989,  Author = {Felsenstein, J.},  Journal = {Cladistics},  Pages = {164--166},  Title = {PHYLIP -- phylogenetic inference package (version 3.2)},  Volume = {5},  Year = {1989}}  @article{Felsenstein1988,  Author = {Felsenstein, J.},  Journal = {Annual Review of Genetics},  Pages = {521--565},  Title = {Phylogenies from molecular sequences: inference and reliability},  Volume = {22},  Year = {1988}}  @article{Felsenstein1985,  Author = {Felsenstein, J.},  Journal = {Evolution},  Pages = {783--791},  Title = {Confidence limits on phylogenies: an approach using the bootstrap},  Volume = {39},  Year = {1985}}  @article{Felsenstein1985a,  Author = {Felsenstein, J.},  Journal = {American Naturalist},  Pages = {1--15},  Title = {Phylogenies and the comparative method},  Volume = {125},  Year = {1985}}  @article{Felsenstein1981,  Author = {Felsenstein, J.},  Journal = {Journal of Molecular Evolution},  Pages = {368--376},  Title = {Evolutionary trees from DNA sequences: a maximum likelihood approach},  Volume = {17},  Year = {1981}}  @article{Felsenstein1978,  Author = {Felsenstein, J.},  Journal = {Systematic Zoology},  Pages = {27--33},  Title = {The number of evolutionary trees},  Volume = {27},  Year = {1978}}  @article{Felsenstein1978a,  Author = {Felsenstein, J.},  Journal = {Systematic Zoology},  Notes = {long branch problem},  Pages = {401--410},  Title = {Cases in which parsimony or compatibility methods will be positively misleading},  Volume = {27},  Year = {1978}}  @article{Felsenstein1973,  Author = {Felsenstein, J.},  Journal = {American Journal of Human Genetics},  Notes = {Brownian motion},  Pages = {471--492},  Title = {Maximum likelihood estimation of evolutionary trees from continuous characters},  Volume = {25},  Year = {1973}}  @article{Felsenstein1996,  Author = {Felsenstein, J. and Churchill, G.A.},  Journal = {Molecular Biology and Evolution},  Pages = {93--104},  Title = {A hidden Markov model approach to variation among sites in rate of evolution},  Volume = {13},  Year = {1996}}  @article{Feng1997,  Author = {Feng, D.F. and Cho, G. and Doolittle, R.F.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {13028--13033},  Title = {Determining divergence times with a protein clock: update and reevaluation},  Volume = {94},  Year = {1997}}  @article{Feng1988,  Author = {Feng, S. and Holland, E.C.},  Journal = {Nature},  Pages = {165-167},  Title = {HIV-1 tat trans-activation requires the loop sequence within TAR},  Volume = {334},  Year = {1988}}  @article{Feng2003,  Author = {Feng, X. and Buell, D.A. and Rose, J.R. and Waddell, P.J.},  Journal = {Journal of Parallel and Distributed Computing},  Pages = {707-718},  Title = {Parallel algorithms for Bayesian phylogenetic inference},  Volume = {63},  Year = {2003}}  @article{Ferguson1973,  Author = {Ferguson, T.S.},  Journal = {Annals of Statistics},  Pages = {209--230},  Title = {A Bayesian analysis of some nonparametric problems},  Volume = {1},  Year = {1973}}  @article{Figlerowicz2000,  Author = {Figlerowicz, M. and Bibillo, A.},  Journal = {RNA},  Pages = {339-351},  Title = {RNA motifs mediating in vivo site-specific nonhomologous recombination in (+) RNA virus enforce in vitro nonhomologous crossovers with HIV-1 reverse transcriptase},  Volume = {6},  Year = {2000}}  @book{Fisher1930,  Address = {Oxford},  Author = {Fisher, R.A.},  Date-Added = {2008-03-28 16:55:14 +1300},  Date-Modified = {2008-03-28 16:56:23 +1300},  Publisher = {Clarendon Press},  Title = {The Genetical Theory of Natural Selection},  Year = {1930}}  @article{Fisher1918,  Author = {Fisher, R.A.},  Date-Added = {2008-03-28 16:52:54 +1300},  Date-Modified = {2008-03-28 16:53:36 +1300},  Journal = {Trans. Roy. Soc. Edinb.},  Pages = {399-433},  Title = {The correlation between relatives on the supposition of Mendelian inheritance},  Volume = {52},  Year = {1918}}  @article{Foca2006,  Author = {Foca, M. and Moye, J. and Chu, C. and Matthews, Y. and Rich, K. and et al},  Journal = {Pediatrics},  Pages = {146--155},  Title = {Gender differences in lymphocyte populations, plasma HIV RNA levels and disease progression in a cohort of children born to women infected with HIV},  Volume = {118},  Year = {2006}}  @article{FOLEY2000,  Abstract = {It is a vexing problem to achieve a consensus about the proper scientific  way to assess population viability for habitat conservation plans.  Rather than a hypothesis-testing approach, here it is proposed to  select population models, estimate extinction parameters, and assess  prediction uncertainty using a pragmatic, empirical Bayesian approach.  The simplest usable models include the effects of population growth,  r; carrying capacity, K; Allee threshold, N(A); and environmental  stochasticity, v(r). Analytic predictions of expected extinction  times are available for such models. Models that are more complex  can be elaborated from this basis. Selection from a hierarchy of  nesting population models can often be done through the evaluation  of parameters. The estimation of the most important extinction parameters  can be undertaken in a variety of ways. Time series can be analyzed  to estimate r(d), v(r), rho, and K. Habitat models and individualistic  population models may help estimate N(A) and K and demographic stochasticity.  Fine-scale biogeography and climatological data may be useful in  the estimation of a variety of parameters. Because it takes many  years to estimate extinction parameters accurately for a given population  of interest, the most efficient estimation procedures are desirable.  I propose the use of prior information from an (as yet nonexistent)  population biology database. The accumulation of local information  through monitoring will improve our estimates allowing adaptive management.  Uncertainty in the estimates will always remain, but it may be quantified  by the posterior distributions. A crude example is discussed using  treefrog population data. Although the motivations, beliefs, and  biases of competing stakeholders will differ, a habitat conservation  plan could accommodate this variation in the prior distributions.  Field experience from monitoring will increasingly clear up any discrepancies  between the opposing beliefs and the real ecosystem. As the world  is an uncertain place and because there is no universal scientific  method, there will always be controversy and surprises. The best  we can do is (1) agree about our prior information, (2) agree about  the strategy of model selection and parameter estimation, and (3)  agree about our strategy for adaptive management. Perhaps the greatest  impediment to such prior agreements for HCPs is the likely paranoia  inspired by the use of unfamiliar statistical methodology. We need  to train students of ecology in a more flexible and deeper understanding  of statistics and philosophy of science.},  Address = {Department of Biological Sciences, California State University, Sacramento, California 95819-6077, USA},  Author = {Foley, P},  Da = {20000509},  Date-Added = {2008-04-13 17:32:20 +1200},  Date-Modified = {2014-07-06 00:57:32 +0000},  Edat = {2000/05/10},  Issn = {0364-152X (Print)},  Jid = {7703893},  Journal = {Environ Manage},  Jt = {Environmental management},  Language = {ENG},  Mhda = {2000/05/10},  Number = {S1},  Own = {NLM},  Pages = {S55-S73},  Pii = {10.1007/s002670010062},  Pmid = {10801990},  Pst = {ppublish},  Pt = {JOURNAL ARTICLE},  Pubm = {Print},  So = {Environ Manage. 2000 Jul;26(S1):S55-S73.},  Stat = {Publisher},  Title = {Problems in Extinction Model Selection and Parameter Estimation.},  Volume = {26},  Year = {2000}}  @article{Foley1994,  Abstract = {Managers of small populations often need to estimate the expected  time to extinction T(e) of their charges. Useful models for extinction  times must be ecologically realistic and depend on measurable parameters.  Many populations become extinct due to environmental stochasticity,  even when the carrying capacity K is stable and the expected growth  rate is positive. A model is proposed that gives T(e) by diffusion  analysis of the log population size n(t) (= log(e) N(t)). The model  population grows according to the equation N(t+1) = R(t)N(t), with  K as a ceiling. Application of the model requires estimation of the  parameters k = logK, r(d) = the expected change in n, v(r) = Variance(log  R), and rho the autocorrelation of the r(t). These are readily calculable  from annual census data (r(d) is trickiest to estimate). General  formulas for T(e) are derived. As a special case, when environmental  fluctuations overwhelm expected growth (that is r(d) almost-equal-to  0), T(e) = 2n0(k - n0/2)/v(r). If the r(t) are autocorrelated, then  the effective variance is v(re) almost-equal-to v(r) (1 + rho)/(1  - rho). The theory is applied to populations of checkerspot butterfly,  grizzly bear, wolf and mountain lion.},  Author = {Foley, P},  Date-Added = {2008-05-23 11:05:18 +1200},  Date-Modified = {2008-05-23 11:06:34 +1200},  Journal = {Conservation Biology},  Pages = {124-137},  Timescited = {0},  Title = {Predicting Extinction Times from Environmental Stochasticity and Carrying Capacity},  Volume = {8},  Year = {1994}}  @techreport{Fonseca2006,  Author = {Fonseca, T. C. O. and Ferreira, M. A. R. and Migon, H. S.},  Institution = {Departamento de M\'etodos Estat\'\i sticos - Universidade Federal do Rio de Janeiro},  Number = {187},  Title = {Objective Bayesian analysis for the Student-t regression model},  Year = {2006}}  @techreport{Forster????,  Author = {Forster, J.J.},  Notes = {model selection},  Title = {Bayesian inference for Poisson and multinomial log-linear models},  Year = {????}}  @book{Foster1995,  Author = {Foster, I.},  Publisher = {Wesley, Addison},  Title = {Designing and Building Parallel Programs},  Year = {1995}}  @other{Foundation2003,  Author = {Foundation, San Francisco AIDS},  Publisher = {Public Policy Department},  Title = {HIV/AIDS statistics},  Year = {2003}}  @other{Foundation2003a,  Author = {Foundation, San Francisco AIDS},  Publisher = {Public Policy Department},  Title = {HIV/AIDS statistics},  Year = {2003}}  @article{Foxman2000,  Author = {Foxman, B. and Barlow, R. and D'Arcy, H. and Gillespie, B. and Sobel, J.D.},  Journal = {Annals of Epidemiology},  Notes = {urosenor},  Pages = {509--515},  Title = {Urinary tract infection: self-reported incidence and associated costs},  Volume = {10},  Year = {2000}}  @article{Fredricks2001,  Author = {Fredricks, D.N. and Relman, D.A.},  Journal = {Journal of Infectious Diseases},  Notes = {id},  Pages = {1299--1237},  Title = {Localization of \textit{Tropheryma whippelii} rRNA in tissues from patients with Whipple's disease},  Volume = {183},  Year = {2001}}  @article{Fredricks1999,  Author = {Fredricks, D.N. and Relman, D.A.},  Journal = {Clinical Infectious Dieases},  Notes = {urosensor},  Pages = {475--486},  Title = {Application of polymerase chain reaction to the diagnosis of infectious diseases},  Volume = {29},  Year = {1999}}  @article{Fredricks1996,  Author = {Fredricks, D.N. and Relman, D.A.},  Journal = {Clinical Microbiology Reviews},  Notes = {id},  Pages = {18--33},  Title = {Sequence-based identification of microbial pathogens: a reconsideration of Koch 's postulates},  Volume = {9},  Year = {1996}}  @article{Friedman2001,  Author = {Friedman, R. and Hughes, A.L.},  Journal = {Genome Research},  Notes = {tetralogy},  Pages = {1842--1847},  Title = {Pattern and timing of gene duplication in animal genomes},  Volume = {11},  Year = {2001}}  @techreport{Fronk????,  Author = {Fronk, E.M.},  Notes = {networks},  Title = {Model selection for DAGs via RJMCMC for the discrete and mixed case},  Year = {????}}  @techreport{Fronk????a,  Author = {Fronk, E.M. and Giudici, P.},  Notes = {networks},  Title = {Markov chain Monte Carlo model selection for DAG models},  Year = {????}}  @article{Frost2005,  Author = {Frost, S.D.W. and Wrin, T. and Smith, D.M. and Kosakovsky-Pond, S.L. and Liu, Y. and Paxinos, E. and Chappey, C. and Galovich, J. and Beauchaine, J. and Petropoulos, C.J. and Little, S.J. and Richman, D.D.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {18514--18519},  Title = {Neutralizing antibody responses drive the evolution of human immunodeficiency virus type 1 envelope during recent HIV infection},  Volume = {102},  Year = {2005}}  @article{Frye1995,  Author = {Frye, M.S. and Hedges, S.B.},  Journal = {Molecular Biology and Evolution},  Pages = {168--176},  Title = {Monophyly of the order Rodentia inferred from mitochondrial DNA sequences of the genes for 12S ribosomal RNA, 16S ribosomal RNA and transfer RNA valine},  Volume = {12},  Year = {1995}}  @article{Fryxell1996,  Author = {Fryxell, K.J.},  Journal = {Trends in Genetics},  Notes = {gene families},  Pages = {364--369},  Title = {The coevolution of gene family trees},  Volume = {12},  Year = {1996}}  @article{fu1994,  Author = {Fu, YX},  Journal = {Genetics},  Number = {2},  Pages = {685},  Publisher = {Genetics Soc America},  Title = {{A phylogenetic estimator of effective population size or mutation rate}},  Volume = {136},  Year = {1994}}  @article{Fuchs1998,  Author = {Fuchs, B.M. and Wallner, G. and Beisker, W. and Schwippl, I. and Ludwig, W. and Amann, R.},  Journal = {Applied and Environmental Microbiology},  Notes = {urosenor},  Pages = {4973--4982},  Title = {Flow cytometric analysis of the in situ accessibility of Escherichia coli 16S rRNA for fluorescently labeled oligonucleotide probes},  Volume = {64},  Year = {1998}}  @article{Fullerton2001,  Author = {Fullerton, S.M. and Carvalho, A.B. and Clark, A.G.},  Journal = {Molecular Biology and Evolution},  Notes = {cg},  Pages = {1139--1142},  Title = {Local rates of recombination are positively correlated with GC content in the human genome},  Volume = {18},  Year = {2001}}  @article{Furnival1974,  Author = {Furnival, G.M. and Wilson, R.W.},  Journal = {Technometrics},  Pages = {499--511},  Title = {Regressions by Leaps and Bounds},  Volume = {16},  Year = {1974}}  @article{Gabrielsson2000,  Author = {Gabrielsson, J. and Jusko, W.J. and Alari, L.},  Journal = {Biopharmaceutics \& Drug Disposition},  Notes = {chang},  Pages = {41--52},  Title = {Modeling of dose-response-time data: four examples of estimating the turnover parameters and generating kinetic functions from response profiles},  Volume = {21},  Year = {2000}}  @article{Ganapathy,  Author = {Ganapathy, G. and Ramachandran, V. and Warnow, T.},  Notes = {HGT},  Title = {Better hill-climbing searches for parsimony}}  @article{Ganeshan1997,  Author = {Ganeshan, S. and Dickover, R.E. and Korber, B.T. and Bryson, Y.J. and Wolinsky, S.M.},  Journal = jv,  Notes = {cr},  Pages = {663--677},  Title = {Human Immunodeficiency virus type 1 genetic evolution in children with different rates of development of disease},  Volume = {71},  Year = {1997}}  @article{Garcia-Vallve2000,  Author = {Garcia-Vallve, S. and Romeu, A. and Palau, J.},  Journal = {Genome Research},  Notes = {HGT},  Pages = {1719--1725},  Title = {Horizontal gene transfer in bacterial and archeal complete genomes},  Volume = {10},  Year = {2000}}  @book{Gardiner2004,  Address = {Berlin},  Author = {Gardiner, C. 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E. and Gu, X. and Suchard, M. A.},  Date-Modified = {2014-07-06 02:07:23 +0000},  Journal = {Molecular Biology and Evolution},  Title = {Time squared: repeated measures on phylogenies},  Year = {revised and resubmitted}}  @article{Guyer1993,  Author = {Guyer, C. and Slowinski, J.B.},  Journal = {Evolution},  Notes = {tree shape},  Pages = {253--263},  Title = {Adaptive radiation and the topology of large phylogenies},  Volume = {47},  Year = {1993}}  @article{Haake2004,  Author = {Haake, D. A. and Suchard, M. A. and Kelley, M. M. and Dundoo, M. and Alt, D. P. and Zuerner, R. L.},  Date-Modified = {2014-07-06 02:10:37 +0000},  Journal = {Journal of Bacteriology},  Pages = {2818--2828},  Title = {Molecular evolution and mosaicism of leptospiral outer membrane proteins involves horizontal DNA transfer},  Volume = {186},  Year = {2004}}  @article{Hagelberg1999,  Author = {Hagelberg, E. and Goldman, N. and Lio, P. and Whelan, S. and Schiefenhovel, W. and Clegg, J.B. and Bowden, D.K.},  Journal = {Proceedings of the Royal Society of London, B},  Notes = {mtDNA recombination},  Pages = {485--492},  Title = {Evidence for mitochondrial DNA recombination in a human population of island Melanesia},  Volume = {266},  Year = {1999}}  @article{Hakoyama2000,  Abstract = {Environmental threats, such as habitat size reduction or environmental  pollution, may not cause immediate extinction of a population but  shorten the expected time to extinction. We develop a method to estimate  the mean time to extinction for a density-dependent population with  environmental fluctuation. We first derive a formula for a stochastic  differential equation model (canonical model) of a population with  logistic growth with environmental and demographic stochasticities.  We then study an approximate maximum likelihood (AML) estimate of  three parameters (intrinsic growth rate r, carrying capacity K, and  environmental stochasticity sigma(2)(e)) from a time series of population  size. The AML estimate of r has a significant bias, but by adopting  the Monte Carlo method, we can remove the bias very effectively (bias-corrected  estimate). We can also determine the confidence interval of the parameter  based on the Monte Carlo method. If the length of the time series  is moderately long (with 40-50 data points), parameter estimation  with the Monte Carlo sampling bias correction has a relatively small  variance. However, if the time series is short (less than or equal  to 10 data points), the estimate has a large variance and is not  reliable. If we know the intrinsic growth rate r, however, the estimate  of K and sigma(2)(e)and the mean extinction time T are reliable even  if only a short time series is available. We illustrate the method  using data for a freshwater fish, Japanese crucian carp (Carassius  auratus subsp.) in Lake Biwa, in which the growth rate and environmental  noise of crucian carp are estimated using fishery records.},  Address = {Department of Biology, Kyushu University, Fukuoka, 812-8581, Japan. [email protected]},  Au = {Hakoyama, H and Iwasa, Y},  Author = {Hakoyama, H and Iwasa, Y},  Ci = {Copyright 2000 Academic Press.},  Da = {20000717},  Date-Added = {2008-04-13 17:32:20 +1200},  Date-Modified = {2008-04-13 17:39:02 +1200},  Dcom = {20000717},  Doi = {10.1006/jtbi.2000.2019},  Edat = {2000/05/19 09:00},  Issn = {0022-5193 (Print)},  Jid = {0376342},  Journal = {J Theor Biol},  Jt = {Journal of theoretical biology},  Language = {eng},  Lr = {20061115},  Mh = {Animals; *Carps; *Computer Simulation; Ecology; Logistic Models; *Population Dynamics; Sensitivity and Specificity; Time Factors; Water Pollution, Chemical},  Mhda = {2000/07/25 11:00},  Number = {3},  Own = {NLM},  Pages = {337--359},  Pii = {S0022-5193(00)92019-8},  Pl = {ENGLAND},  Pmid = {10816359},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Sb = {IM},  So = {J Theor Biol. 2000 Jun 7;204(3):337-59.},  Stat = {MEDLINE},  Title = {Extinction risk of a density-dependent population estimated from a time series of population size.},  Volume = {204},  Year = {2000},  Bdsk-Url-1 = {http://dx.doi.org/10.1006/jtbi.2000.2019}}  @book{Haldane1932,  Address = {London},  Author = {Haldane, J. B. S},  Call-Number = {QH366},  Date-Added = {2008-03-28 17:08:09 +1300},  Date-Modified = {2008-03-28 17:08:21 +1300},  Dewey-Call-Number = {575.01},  Genre = {Evolution (Biology)},  Library-Id = {32033284},  Publisher = {Longmans, Green and co.},  Title = {The causes of evolution},  Year = {1932}}  @article{Hall2002,  Author = {Hall, M.A. Leverstein-van and Box, A.T.A. and Blok, H.E.M. and Pauuw, A. and Fluit, A.C. and Verhoef, J.},  Journal = {The Journal of Infectious Diseases},  Pages = {49--56},  Title = {Evidence of extensive interspecies transfer of integron-mediated antimicrobial resistance genes among multidrug-resistant Enterobacteriaceae in a clinical setting},  Volume = {186},  Year = {2002}}  @article{Hamada2003,  Author = {Hamada, H. and Pohl, A. and Spiegelman, C. and Wendelberger, J.},  Journal = {Journal of Quality Technology},  Notes = {calibration},  Pages = {194--205},  Title = {A Bayesian approach to calibration intervals and properly calibrated tolerance intervals},  Volume = {35},  Year = {2003}}  @article{Hamilton2003,  Author = {Hamilton, M.B. and Braverman, J.M. and Soria-Hernanz, D.F.},  Journal = {Molecular Biology and Evolution},  Pages = {1710--1721},  Title = {Patterns and relative rates of nucleotide and insertion/deletion evolution in six chloroplast intergenic regions in New World species of the Lecythidaceae},  Volume = {20},  Year = {2003}}  @techreport{Han2001,  Author = {Han, C. and Carlin, B.P.},  Title = {MCMC methods for computing Bayes factors: a compartive review},  Year = {2001}}  @article{Handt1998,  Author = {Handt, O. and Meyer, S. and von Haeseler, A.},  Journal = {Nucleic Acids Research},  Pages = {126--129},  Title = {Compilation of human mtDNA control region sequences},  Volume = {26},  Year = {1998}}  @article{Hanson2001,  Author = {Hanson, K.M.},  Journal = {Proceedings of SPIE},  Title = {Markov chain Monte Carlo posterior sampling with the Hamiltonian method},  Year = {2001}}  @article{Harding1971,  Author = {Harding, E.F.},  Journal = {Advances in Applied Probability},  Notes = {tree shape},  Pages = {44--77},  Title = {The probabilities of rooted tree-shapes generated by random bifurcation},  Volume = {3},  Year = {1971}}  @techreport{Hartemink????,  Author = {Hartemink, A.J. and Gifford, D.K. and Jaakkola, T.S. and Young, R.A.},  Notes = {networks},  Title = {Using graphical models and genomic expression data to statistically validate models of genetic regulatory networks},  Year = {????}}  @article{Hartley2005,  Author = {Hartley, O. and Klasse, P.J. and Sattentau, Q.J. and Moore, J.P.},  Journal = {AIDS Research and Human Retroviruses},  Pages = {171--189},  Title = {V3: HIV's Switch-Hitter},  Volume = {21},  Year = {2005}}  @article{Harville1976,  Author = {Harville, D.},  Journal = {Annals of Statistics},  Pages = {384--395},  Title = {Extension of the Gauss-Markov theorem to include the estimation of random effects},  Volume = {4},  Year = {1976}}  @article{Hasegawa1992,  Author = {Hasegawa, M. and Cao, Y. and Adachi, J. and Yano, T.},  Journal = {Nature},  Pages = {595},  Title = {Rodent polyphyly},  Volume = {355},  Year = {1992}}  @article{Hasegawa1985,  Author = {Hasegawa, M. and Kishino, H. and Yano, T.},  Journal = {Journal of Molecular Evolution},  Pages = {160--174},  Title = {Dating the human-ape splitting by a molecular clock of mitochondrial DNA},  Volume = {22},  Year = {1985}}  @article{Hasegawa1993,  Author = {Hasegawa, M. and Rienzo, A.D. and Kocher, T.D. and Wilson, A. C.},  Date-Modified = {2014-07-06 03:41:21 +0000},  Journal = {Journal of Molecular Evolution},  Pages = {347--354},  Title = {Toward a more accurate time scale for the human mitochondrial DNA tree},  Volume = {37},  Year = {1993}}  @book{Hastie2001,  Author = {Hastie, T. and Tibshirani, R. and Friedman, J.H.},  Publisher = {Springer},  Title = {The Elements of Statistical Learning},  Year = {2001}}  @article{Hastings1970,  Author = {Hastings, W.K.},  Journal = {Biometrika},  Pages = {97--109},  Title = {Monte Carlo sampling methods using Markov chains and their applications},  Volume = {57},  Year = {1970}}  @article{Hayasaka1988,  Author = {Hayasaka, K. and Gojobori, K.T. and Horai, S.},  Journal = {Molecular Biology and Evolution},  Pages = {626--644},  Title = {Molecular phylogeny and evolution of primate mitochondrial DNA},  Volume = {5},  Year = {1988}}  @article{He2007,  Abstract = {Seasonal oscillations in birth rates are ubiquitous in human populations.  These oscillations might play an important role in infectious disease  dynamics because they induce seasonal variation in the number of  susceptible individuals that enter populations. We incorporate seasonality  of birth rate into the standard, deterministic susceptible-infectious-recovered  (SIR) and susceptible-exposed-infectious-recovered (SEIR) epidemic  models and identify parameter regions in which birth seasonality  can be expected to have observable epidemiological effects. The SIR  and SEIR models yield similar results if the infectious period in  the SIR model is compared with the infected period (the sum of the  latent and infectious periods) in the SEIR model. For extremely transmissible  pathogens, large amplitude birth seasonality can induce resonant  oscillations in disease incidence, bifurcations to stable multi-year  epidemic cycles, and hysteresis. Typical childhood infectious diseases  are not sufficiently transmissible for their asymptotic dynamics  to be likely to exhibit such behaviour. However, we show that fold  and period-doubling bifurcations generically occur within regions  of parameter space where transients are phase-locked onto cycles  resembling the limit cycles beyond the bifurcations, and that these  phase-locking regions extend to arbitrarily small amplitude of seasonality  of birth rates. Consequently, significant epidemiological effects  of birth seasonality may occur in practice in the form of transient  dynamics that are sustained by demographic stochasticity.},  Address = {Department of Mathematics and Statistics, McMaster University, Hamilton, Ont., Canada L8S 4K1. [email protected]},  Au = {He, D and Earn, DJ},  Author = {He, Daihai and Earn, David J D},  Da = {20070813},  Date-Added = {2008-04-13 17:20:00 +1200},  Date-Modified = {2008-04-13 17:23:48 +1200},  Dcom = {20071120},  Dep = {20070507},  Doi = {10.1016/j.tpb.2007.04.004},  Edat = {2007/06/26 09:00},  Issn = {0040-5809 (Print)},  Jid = {0256422},  Journal = {Theor Popul Biol},  Jt = {Theoretical population biology},  Language = {eng},  Mh = {*Birth Rate; Canada/epidemiology; Communicable Diseases/*epidemiology; Disease Progression; Disease Susceptibility; Humans; Models, Statistical; *Seasons; Sentinel Surveillance},  Mhda = {2007/12/06 09:00},  Number = {2},  Own = {NLM},  Pages = {274--291},  Pii = {S0040-5809(07)00041-X},  Pl = {United States},  Pmid = {17588629},  Pst = {ppublish},  Pt = {Journal article},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Theor Popul Biol. 2007 Sep;72(2):274-91. Epub 2007 May 7.},  Stat = {MEDLINE},  Title = {Epidemiological effects of seasonal oscillations in birth rates.},  Volume = {72},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tpb.2007.04.004}}  @article{Heckman2000,  Author = {Heckman, N.E. and Ramsay, J.O.},  Journal = {Canadian Journal of Statistics},  Notes = {expression},  Pages = {241--258},  Title = {Penalized regression with model-based penalties},  Volume = {28},  Year = {2000}}  @article{Hedges1990,  Author = {Hedges, S.B. and Moberg, K.D. and Maxson, L.R.},  Journal = {Molecular Biology and Evolution},  Notes = {alignment; rRNA},  Pages = {607--633},  Title = {Tetrapod phylogeny inferred from 18S and 28S ribosomal RNA sequences and a review of the evidence for Amniote relationships},  Volume = {7},  Year = {1990}}  @article{Heiberger1978,  Author = {Heiberger, R. M.},  Date-Modified = {2014-07-06 02:40:44 +0000},  Journal = {Applied Statistics},  Pages = {199--206},  Title = {Algorithm AS 127. 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A.},  Date-Modified = {2014-07-06 00:57:46 +0000},  Journal = {Genome Biology},  Notes = {gene families},  Pages = {1002.1--1002.3},  Title = {Orthologs and paralogs -- we need to get it right},  Volume = {2},  Year = {2001}}  @article{Jetzt2000,  Author = {Jetzt, A.E. and Yu, H. and Klarmann, G.J. and Ron, Y. and Preston, B.D. and Dougherty, J.P.},  Journal = {Journal of Virology},  Pages = {1234-1240},  Title = {High rate of recombination throughout the human immunodeficiency virus type 1 genome},  Volume = {74},  Year = {2000}}  @techreport{Johnson2000,  Author = {Johnson, V.E.},  Institution = {ISDS, Duke University},  Title = {Posterior distributions on normalizing constants},  Year = {2000}}  @incollection{Jukes1969,  Address = {New York},  Author = {Jukes, T. and Cantor, C.},  Booktitle = {Mammaliam Protein Metabolism},  Editor = {Munro, H.N.},  Pages = {21--132},  Publisher = {Academic Press},  Title = {Evolution of protein molecules},  Year = {1969}}  @article{Kaliki2000,  Author = {Kaliki, V. and Day, N.K. and Dinglasa, E. and James-Yarish, M. and Hitchcock, R. and Skapura, D. and Chinta, A. and Johnson, L. and Andreopolis, A. and Rey, A. and Good, R.A. and Haraguchi, S.},  Journal = il,  Notes = {cr},  Pages = {173--176},  Title = {Emergence of HIV-1 variants containing codon insertions and deletions in the beta3-beta4 hairpin loop domain of reverse transcriptase},  Volume = {74},  Year = {2000}}  @article{Kalish2004,  Author = {Kalish, M.L. and Robbins, K.E. and Pieniazek, D. and Schaefer, A. and Nzilambi, N. and Quinn, T. and Louis, M.R. St and Youngpairoj, A.S. and Phillips, J. and Jaffe, H.W. and Folks, T.M.},  Journal = {Emerging Infectious Disease},  Pages = {1227--1234},  Title = {Recombinant viruses and early global HIV-1 epidemic},  Volume = {10},  Year = {2004}}  @article{Kampinga1997,  Author = {Kampinga, G. and Simonon, A. and de Perre, P. Van and Karita, E. and Msellati, P. and Goudsmit, J.},  Journal = {Journal of Virology},  Pages = {63--76},  Title = {Primary infections with HIV-1 of women and their offspring in Rwanda: findings of heterogeneity at seroconversion, coinfection and recombinants of HIV-1 subtypes A and C},  Volume = {227},  Year = {1997}}  @article{Karlin1993,  Author = {Karlin, S. and Altschul, S.F.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Notes = {urosenor,blast},  Pages = {5873--5877},  Title = {Applications and statistics for multiple high-scoring segments in molecular sequences},  Volume = {90},  Year = {1993}}  @article{Karlsson1999,  Author = {Karlsson, A.C. and Gaines, H. and Sallberg, M. and Lindback, S. and Sonnerborg, A.},  Journal = jv,  Notes = {cr},  Pages = {6191--196},  Title = {Reappearance of founder virus sequence in HIV-1 infected patients},  Volume = {73},  Year = {1999}}  @article{Kaslow1987,  Author = {Kaslow, R.A. and Ostrow, D.G. and Detels, R. and Phair, J.P. and Polk, B.F and R.C. Rinaldo\, Jr},  Journal = {American Journal of Epidemiology},  Pages = {310--318},  Title = {The multicenter AIDS cohort study: rationale, organization and selected characteristics of the participants},  Volume = {126},  Year = {1987}}  @article{Kass1995,  Author = {Kass, R. E. and Raftery, A. E.},  Date-Modified = {2014-12-04 01:09:21 +0000},  Journal = {Journal of the American Statistical Association},  Pages = {773--795},  Title = {Bayes factors},  Volume = {90},  Year = {1995}}  @article{Kateri2001,  Author = {Kateri, M. and Papaioannou, T. and Dellaportas, P.},  Journal = {Sankhya},  Notes = {model selection},  Pages = {270--285},  Title = {Bayesian analysis of correlated proportions},  Volume = {63},  Year = {2001}}  @article{Kato1999,  Author = {Kato, K. and Sato, H. and Takebe, Y},  Journal = {JV},  Pages = {5520--5526},  Title = {Role of naturally occuring basic amino acid substitutions in the HIV-1E envelope on coreceptor usage and cell tropism},  Volume = {73},  Year = {1999}}  @article{Ke2001,  Author = {Ke, C. and Wang, Y.},  Journal = {Journal of the American Statistical Assocation},  Notes = {splines},  Pages = {1272--1298},  Title = {Semi-parametric nonlinear mixed effects models and their applications},  Volume = {96},  Year = {2001}}  @article{Ke2000,  Author = {Ke, D. and Boissinot, M. and Huletsky, A. and Picard, F.J. and Frenette, J. and Ouellette, M. and P.H. and Roy and Bergeron, M.G.},  Journal = {Journal of Bacteriology},  Pages = {6913--6920},  Title = {Evidence for horizontal gene transfer in evolution of elongation factor Tu in enterococci},  Volume = {182},  Year = {2000}}  @article{Keightley2004,  Author = {Keightley, P.D. and Johnson, T.},  Journal = {Genome Research},  Notes = {alignment; indel},  Pages = {442--450},  Title = {MCALIGN: stochastic alignment of noncoding DNA sequences based on an evolutionary model of sequence evolution},  Volume = {14},  Year = {2004}}  @article{Kellam1997,  Author = {Kellam, P. and Larder, B.A.},  Journal = jv,  Notes = {cr},  Pages = {669--674},  Title = {retroviral recombination can lead to linkage of reverse transcriptase mutatnts that confer increased idovudine resistance},  Volume = {69},  Year = {1997}}  @article{Kellam1995,  Author = {Kellam, P. and Larder, B.A.},  Journal = {Journal of Virology},  Pages = {669--674},  Title = {Retroviral recombination can lead to linkage of reverse transcriptase mutations that confer increased zidovudine resistance},  Volume = {69},  Year = {1995}}  @article{Kelley2003,  Author = {Kelley, J.K. and Williamson, S. and Orive, M.E. and Smith, M.S. and Holt, R.D.},  Journal = {American Naturalist},  Pages = {14--28},  Title = {Linking dynamical and population genetics models of persistent viral infection},  Volume = {162},  Year = {2003}}  @article{Kelly2003,  Abstract = {This article develops a theoretical framework to link dynamical and  population genetic models of persistent viral infection. This linkage  is useful because, while the dynamical and population genetic theories  have developed independently, the biological processes they describe  are completely interrelated. Parameters of the dynamical models are  important determinants of evolutionary processes such as natural  selection and genetic drift. We develop analytical methods, based  on coupled differential equations and Markov chain theory, to predict  the accumulation of genetic diversity within the viral population  as a function of dynamical parameters. These methods are first applied  to the standard model of viral dynamics and then generalized to consider  the infection of multiple host cell types by the viral population.  Each cell type is characterized by specific parameter values. Inclusion  of multiple cell types increases the likelihood of persistent infection  and can increase the amount of genetic diversity within the viral  population. However, the overall rate of gene sequence evolution  may actually be reduced.},  Address = {Department of Ecology and Evolutionary Biology, University of Kansas, Lawrence, Kansas 66045, USA. [email protected]},  Au = {Kelly, JK and Williamson, S and Orive, ME and Smith, MS and Holt, RD},  Author = {Kelly, John K and Williamson, Scott and Orive, Maria E and Smith, Marilyn S and Holt, Robert D},  Da = {20030711},  Date-Added = {2008-04-13 17:03:57 +1200},  Date-Modified = {2008-04-13 17:04:30 +1200},  Dcom = {20031009},  Dep = {20030612},  Edat = {2003/07/12 05:00},  Gr = {1 R01 GM60792-01A1/GM/United States NIGMS},  Issn = {0003-0147 (Print)},  Jid = {2984688R},  Journal = {Am Nat},  Jt = {The American naturalist},  Language = {eng},  Lr = {20071114},  Mh = {Evolution; *Genetics, Population; Markov Chains; *Models, Biological; Variation (Genetics); Virus Diseases/*genetics},  Mhda = {2003/10/10 05:00},  Number = {1},  Own = {NLM},  Pages = {14--28},  Pii = {AN020270},  Pl = {United States},  Pmid = {12856234},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Am Nat. 2003 Jul;162(1):14-28. Epub 2003 Jun 12.},  Stat = {MEDLINE},  Title = {Linking dynamical and population genetic models of persistent viral infection.},  Volume = {162},  Year = {2003}}  @article{Kemal2003,  Author = {Kemal, K.S. and Foley, B. and Burger, H. and Anastos, K. and Minkoff, H. and Kitchen, C. and Philpott, S.M. and Gao, W. and Robison, E. and Holman, S. and Dehner, C. and Beck, S. and Meyer, W.A. and Landay, A. and Kovacs, A. and Bremer, J. and Weiser, B.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {12972--12977},  Title = {HIV-1 in genital tract and plasma of women: compartmentalization of viral sequences, coreceptor usage and glycosylation},  Volume = {100},  Year = {2003}}  @article{Kerr2001,  Author = {Kerr, M.K. and Churchill, G.A.},  Journal = {Proceedings of the National Academies of Science, USA},  Notes = {yeast expression},  Pages = {8961--8965},  Title = {Bootstrapping cluster analysis: assessing the reliability of conclusions from microarray experiments},  Volume = {98},  Year = {2001}}  @article{Kijak2002,  Author = {Kijak, G.H. and Simon, V. and Balfe, P. and Vanderhoeven, J. and Pampuro, S.E. and Zala, C. and Ochoa, C. and Cahn, P. and Markowitz, M. and Salomon, H.},  Journal = {Journal of Virology},  Pages = {7000-7009},  Title = {Origin of human immunodeficiency virus type 1 quasispecies emerging after antiretroviral treatment interruption in patients with therapeutic failure},  Volume = {76},  Year = {2002}}  @article{Killian2001,  Author = {Killian, J.K. and Buckley, T.R. and Stewart, N. and Munday, B.L. and Jirtle, R.L.},  Journal = {Mammalian Genetics},  Keywords = {hierarchical},  Pages = {513--517},  Title = {Marsupials and Eutherians reunited: genetic evidence for the Theria hypothesis of mammalian evolution},  Volume = {12},  Year = {2001}}  @article{Kim2000,  Author = {Kim, C.B. and Amemiya, C. and Bailey, W. and Kawasaki, K. and Mezey, J. and Miller, W. and Minoshima, S. and Shimizu, N. and Wagner, G. and Ruddle, F.},  Journal = {PNAS},  Notes = {hox phylogeny, tetralogy},  Pages = {1655--1660},  Title = {Hox cluster genomics in the horn shark, Heterodontus francisci},  Volume = {97},  Year = {2000}}  @article{Kimura1980,  Author = {Kimura, M.},  Journal = {Journal of Molecular Evolution},  Pages = {111--120},  Title = {A simple model for estimating evolutionary rates of base substitutions through comparative studies of nucleotide sequences},  Volume = {16},  Year = {1980}}  @article{King1975,  Author = {King, M. C. and Wilson, A. C.},  Date-Modified = {2014-07-06 03:42:51 +0000},  Journal = {Science},  Notes = {107--116},  Title = {Evolution at two levels in humans and chimpanzees},  Volume = {188},  Year = {1975}}  @article{Kingman2000,  Author = {Kingman, J.F.C.},  Journal = {Genetics},  Pages = {1461--1463},  Title = {Origins of the coalescent: 1974-1982},  Volume = {156},  Year = {2000}}  @article{Kirkpatrick1993,  Author = {Kirkpatrick, M. and Slatkin, M.},  Journal = {Evolution},  Notes = {tree shape},  Pages = {1171--1181},  Title = {Searching for evolutionary patterns in the shape of a phylogenetic tree},  Volume = {47},  Year = {1993}}  @article{Kirkpatrick1983,  Author = {Kirkpatrick, S. and Gelatt, C.D. and Wecci, M.P.},  Journal = {Science},  Pages = {671--680},  Title = {Optimization by simulated annealing},  Volume = {220},  Year = {1983}}  @article{Kitchen2004,  Author = {Kitchen, C. M. R. and Philpott, S. and Burger, H. and Weiser, B. and Suchard, M. A.},  Date-Modified = {2014-07-06 02:34:27 +0000},  Journal = {Journal of Virology},  Pages = {11296--11302},  Title = {Bayesian analysis of viral evolution: shared patterns in HIV-1 coreceptor utilization during antiretroviral therapy},  Volume = {78},  Year = {2004}}  @article{Kitcheninpress,  Author = {Kitchen, C. M. R. and Suchard, M. A. and Liu, J. and Hoh, R. and Kuritzkes, D. and Deeks, S. G.},  Date-Modified = {2014-07-06 02:33:43 +0000},  Journal = {AIDS Research and Human Retroviruses},  Title = {Continued evolution in \textit{gp41} after interruption of enfuviritide in patients with advanced HIV disease},  Year = {in press}}  @article{Kjems1991,  Author = {Kjems, J. and Brown, M. and Chang, D. and Sharp, S.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {683-687},  Title = {Structural analysis of the interaction between the human immunodeficiency virus Rev protein and the Rev response element},  Volume = {88},  Year = {1991}}  @article{Klevytska2002,  Author = {Klevytska, A.M. and Miracna, M.R. and Guay, L. and Becker-Pergola, G. and Furtado, M. and Zhang, L. and Jackson, J.B. and Eshleman, S.H.},  Journal = {AIDS Research and Human Retroviruses},  Pages = {791--796},  Title = {Analysis of length variation in the V1-V2 region of \textit{env} in nonsubtype B HIV type 1 from Uganda},  Volume = {18},  Year = {2002}}  @article{Kluge1989,  Author = {Kluge, A.G.},  Journal = {Systematic Zoology},  Pages = {7--25},  Title = {A concern for evidence and a phylogenetic hypothesis of relationships among \textit{Epicates} (Boidae, Serpentes)},  Volume = {38},  Year = {1989}}  @article{Knorr-Held2002,  Author = {Knorr-Held, L. and Rue, H.},  Journal = {Scandinavian Journal of Statistics},  Pages = {597-614},  Title = {On block updating in Markov random field models for disease mapping},  Volume = {29},  Year = {2002}}  @article{Kolzsch2007,  Abstract = {1. During the last centuries, the breeding range of the great snipe  Gallinago media has declined dramatically in the western part of  its distribution. To examine present population dynamics in the Scandinavian  mountains, we collected and analysed a 19-year time series of counts  of great snipe males at leks in central Norway, 1987-2005. 2. The  population showed large annual fluctuations in the number of males  displaying at lek sites (range 45-90 males at the peak of the mating  season), but no overall trend. 3. We detected presence of direct  density-dependent mechanisms regulating this population. Inclusion  of the density-dependent term in a Ricker-type model significantly  improved the fit with observed data (evaluated with Parametric Bootstrap  Likelihood Ratio tests and Akaike's Information Criterion for small  sample size). 4. An analysis of (a number of a priori likely) environmental  covariates suggests that the population dynamics were affected by  conditions influencing reproduction and survival of offspring during  the summer, but not by conditions influencing survival at the wintering  grounds in Africa. This is in contrast to many altricial birds breeding  in the northern hemisphere, and supports the idea that population  dynamics of migratory nidifugous birds are more influenced by conditions  during reproduction. 5. Inclusion of these external factors into  our model improved the detectability of density dependence. This  illustrates that allowing for external effects may increase statistical  power of density dependence tests and thus be of particular importance  in relatively short time series. 6. In our best model of the population  dynamics, two likely density-independent offspring survival covariates  explained 47.3% of the variance in great snipe numbers (predation  pressure estimated by willow grouse reproductive success and food  availability estimated by the amount of precipitation in June), whereas  density dependence explained 35.5%. Demographic stochasticity and  unidentified environmental stochasticity may account for the remaining  17.2%.},  Address = {Department of Physics, AGNLD, University of Potsdam, Am Neuen Palais 10, 14469 Potsdam, Germany. [email protected]},  Au = {Kolzsch, A and Saether, SA and Gustafsson, H and Fiske, P and Hoglund, J and Kalas, JA},  Author = {Kolzsch, Andrea and Saether, Stein Are and Gustafsson, Henrik and Fiske, Peder and Hoglund, Jacob and Kalas, John Atle},  Da = {20070622},  Date-Added = {2008-04-13 17:20:00 +1200},  Date-Modified = {2008-04-13 17:24:54 +1200},  Dcom = {20070925},  Doi = {10.1111/j.1365-2656.2007.01246.x},  Edat = {2007/06/23 09:00},  Issn = {0021-8790 (Print)},  Jid = {0376574},  Journal = {J Anim Ecol},  Jt = {The Journal of animal ecology},  Language = {eng},  Mh = {Animal Migration/*physiology; Animals; *Breeding; Charadriiformes/growth \& development/*physiology; Environment; Female; Male; Norway; Population Density; Population Dynamics; *Predatory Behavior; Seasons; Sex Ratio; Stochastic Processes},  Mhda = {2007/09/26 09:00},  Number = {4},  Own = {NLM},  Pages = {740--749},  Pii = {JAE1246},  Pl = {England},  Pmid = {17584380},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Sb = {IM},  So = {J Anim Ecol. 2007 Jul;76(4):740-9.},  Stat = {MEDLINE},  Title = {Population fluctuations and regulation in great snipe: a time-series analysis.},  Volume = {76},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1365-2656.2007.01246.x}}  @article{Kong2003,  Author = {Kong, A. and McCullagh, P. and Meng, X.-L. and Nicolae, D. and Tan, Z.},  Journal = {Journal of the Royal Statistical Society, Series B},  Pages = {585-618},  Title = {A theory of statistical models for Monte Carlo integration},  Volume = {65},  Year = {2003}}  @article{Koonin2001,  Author = {Koonin, E.V. and Makarova, K.S. and Aravind, L.},  Journal = {Annual Review of Microbiology},  Notes = {HGT},  Pages = {709--742},  Title = {Horizontal gene transfer in prokaryotes: quantification and classification},  Volume = {55},  Year = {2001}}  @incollection{Korber1998,  Address = {Los Alamos, NM},  Author = {Korber, B.T. and Foley, B.T. and Kuiken, C.L. and Pillai, S.K. and Sodroski, J.G.},  Booktitle = {Human Retroviruses and AIDS 1998},  Editor = {Korber, B. and Kuiken, C. and Foley, B. and Hahn, B. and McCutchan, F. and Mellors, J. and Sodroski, J.},  Pages = {102--111},  Publisher = {Theoretical Biology and Biophysics Group, Los Alamos National Laboratory},  Title = {Numbering positions in HIV relative to HXB2},  Year = {1998}}  @article{Korber2001,  Author = {Korber, B. and Gaschen, B. and Yusim, K. and Thakallapally, R. and Kesmir, C. and Detours, V.},  Journal = {British Medical Bulletin},  Pages = {19--42},  Title = {Evolutionary and immunological implications of contemporary HIV-1 variation},  Volume = {58},  Year = {2001}}  @article{Korber1998a,  Author = {Korber, B.T. and Theiler, J. and Wolinsky, S.},  Journal = sc,  Notes = {cr},  Pages = {1868--1871},  Title = {Limitations of a Molecular clock to the considerations of the origin of HIV-1},  Volume = {280},  Year = {1998}}  @article{Koski2001,  Author = {Koski, L.B. and Golding, G.B.},  Journal = {Journal of Molecular Evolution},  Pages = {587--599},  Title = {The closest BLAST hit is often not the nearest neighbor},  Volume = {52},  Year = {2001}}  @article{Koski2001a,  Author = {Koski, L.B. and Morton, R.A. and Golding, G.B.},  Journal = {Molecular Biology and Evolution},  Notes = {HGT},  Pages = {404--412},  Title = {Codon bias and base composition are poor indicators of horizontally transferred genes},  Volume = {18},  Year = {2001}}  @article{Kotsopoulou2000,  Author = {Kotsopoulou, E. and Kim, V.N. and Kingsman, A.J. and Kingsman, S.M. and Mitrophanous, K.A.},  Journal = {Journal of Virology},  Pages = {4839--4852},  Title = {A Rev-independent human immunodeficiency virus type 1 (HIV-1)-based vector that exploits a codon-optimized HIV-1 gag-pol gene},  Volume = {74},  Year = {2000}}  @article{Kramers1940,  Author = {Kramers, H.A.},  Date-Added = {2008-03-28 16:39:47 +1300},  Date-Modified = {2008-03-28 16:40:33 +1300},  Journal = {Physica},  Number = {4},  Pages = {284-304},  Title = {Brownian motion in a field of force and the diffusion model of chemical reactions},  Volume = {7},  Year = {1940}}  @article{Kroes1999,  Author = {Kroes, I. and Lepp, P.W. and Relman, D.A.},  Journal = {PNAS},  Pages = {14547--14552},  Title = {Bacterial diversity within the human subgingival crevice},  Volume = {96},  Year = {1999}}  @article{Krone1997,  Author = {Krone, S.M. and Neuhauser, C.},  Journal = {Theoretical Population Biology},  Pages = {210--237},  Title = {Ancestral processes with selection},  Volume = {51},  Year = {1997}}  @article{Kuhner1994,  Author = {Kuhner, M. K. and Felsenstein, J.},  Date-Modified = {2014-07-06 01:58:23 +0000},  Journal = {Molecular Biology and Evolution},  Pages = {459--468},  Title = {A simulation comparison of phylogeny algorithms under equal and unequal evolutionary rates},  Volume = {11},  Year = {1994}}  @article{Kuhner1998,  Author = {Kuhner, M. K. and Yamato, J. and Felsenstein, J.},  Date-Modified = {2014-07-06 01:57:54 +0000},  Journal = {Genetics},  Pages = {429--434},  Title = {Maximum likelihood estimation of population growth rates based on the coalescent},  Volume = {149},  Year = {1998}}  @article{kuhner2000,  Author = {Kuhner, M. K. and Yamato, J. and Felsenstein, J.},  Date-Modified = {2014-07-06 01:35:36 +0000},  Journal = {Genetics},  Number = {3},  Pages = {1393},  Publisher = {Genetics Soc America},  Title = {{Maximum likelihood estimation of recombination rates from population data}},  Volume = {156},  Year = {2000}}  @article{Kuhner1995,  Author = {Kuhner, M. K. and Yamato, J. and Felsenstein, J.},  Date-Modified = {2014-07-06 01:58:04 +0000},  Journal = {Genetics},  Pages = {1421--1430},  Title = {Estimating effective population size and mutation rate from sequence data using Metropolis-Hastings sampling},  Volume = {140},  Year = {1995}}  @article{Kuo1998,  Author = {Kuo, L. and Mallick, B.},  Journal = {Sankhya B},  Notes = {model selection},  Pages = {65--81},  Title = {Variable selection for regression models},  Volume = {60},  Year = {1998}}  @techreport{Kuo1998a,  Author = {Kuo, L. and Mallick, B.},  Notes = {model selection},  Title = {Variable selection for regression models},  Year = {1998}}  @article{Kuwata1997,  Author = {Kuwata, T. and Miyazaki, Y. and Igarashi, T. and Takehisa, J. and Hayami, M.},  Journal = {Journal of Virology},  Pages = {7088--7091},  Title = {The rapid spread of recombinants during a natural in vitro infection with two human immunodeficiency virus type 1 strains},  Volume = {71},  Year = {1997}}  @article{Ladoukakis2001,  Author = {Ladoukakis, E.D. and Zouros, E.},  Journal = {Molecular Biology and Evolution},  Pages = {1168--1175},  Title = {Direct evidence for homologous recombination in Mussel (\textit{Mytilus galloprovincialis}) mitochondrial DNA},  Volume = {18},  Year = {2001}}  @article{Ladoukakis2001a,  Author = {Ladoukakis, E.D. and Zouros, E.},  Journal = {Molecular Biology and Evolution},  Pages = {2127--2131},  Title = {Recombination in animal mitochondrial DNA: evidence from published sequences},  Volume = {18},  Year = {2001}}  @article{Lahn1997,  Author = {Lahn, B.T. and Page, D.C.},  Journal = {Science},  Pages = {675--680},  Title = {Functional coherence of the human Y chromosome},  Volume = {278},  Year = {1997}}  @article{Lai1992,  Author = {Lai, M.M.C.},  Journal = {Microbiol Review},  Pages = {61-79},  Title = {RNA recombination in animal and plan viruses},  Volume = {56},  Year = {1992}}  @article{Laird1978,  Author = {Laird, N.},  Journal = {Journal of the American Statistical Association},  Pages = {805--811},  Title = {Nonparametric maximum likelihood estimation of a mixture distribution},  Volume = {73},  Year = {1978}}  @article{Laird1982,  Author = {Laird, N.M. and Ware, J.H.},  Journal = {Biometrics},  Pages = {963--974},  Title = {Random-effects models for longitudinal data},  Volume = {38},  Year = {1982}}  @article{Lake1998,  Author = {Lake, J.A.},  Journal = {Molecular Biology and Evolution},  Pages = {1224--1231},  Title = {Optimally recovering rate variation information from genomes and sequences: pattern filtering},  Volume = {15},  Year = {1998}}  @article{Lake1994,  Author = {Lake, J.A.},  Journal = {PNAS, USA},  Pages = {1455--1459},  Title = {Reconstructing evolutionary trees from DNA and protein sequences: paralinear distances},  Volume = {91},  Year = {1994}}  @article{Lake1991,  Author = {Lake, J.A.},  Journal = {Molecular Biology and Evolution},  Notes = {alignment},  Pages = {378--385},  Title = {The order of sequence alignment can bias the selection of tree topology},  Volume = {8},  Year = {1991}}  @article{Lake1988,  Author = {Lake, J.A.},  Journal = {Nature},  Pages = {184--186},  Title = {Origin of the eukaryotic nucleus determined by rate-invariant analysis of rRNA sequences},  Volume = {331},  Year = {1988}}  @article{Lake1987,  Author = {Lake, J.A.},  Journal = {Molecular Biology and Evolution},  Pages = {167--191},  Title = {A rate-independent technique for analysis of nucleic acid sequences: evolutionary parsimony},  Volume = {4},  Year = {1987}}  @incollection{Lake1996,  Address = {Cambridge, UK},  Author = {Lake, J.A. and Rivera, M.C.},  Booktitle = {Evolution of Microbial Life},  Editor = {Roberts, D.M. and Sharp, P. and Alderson, G. and Collins, M.A.},  Pages = {87--108},  Publisher = {Cambridge University Press},  Title = {The prokaryotic ancestry of eukaryotes},  Year = {1996}}  @article{Lambert2006,  Abstract = {We link two-allele population models by Haldane and Fisher with Kimura's  diffusion approximations of the Wright-Fisher model, by considering  continuous-state branching (CB) processes which are either independent  (model I) or conditioned to have constant sum (model II). Recent  works by the author allow us to further include logistic density-dependence  (model III), which is ubiquitous in ecology. In all models, each  allele (mutant or resident) is then characterized by a triple demographic  trait: intrinsic growth rate r, reproduction variance sigma and competition  sensitivity c. Generally, the fixation probability u of the mutant  depends on its initial proportion p, the total initial population  size z, and the six demographic traits. Under weak selection, we  can linearize u in all models thanks to the same master formula u  = p + p(1-p )g(r)s(r) + g(sigma)s(sigma) + g(c)s(c) + o(s(r), s(sigma)  s(c)), where s(r) = r' - r, s(sigma) = sigma - sigma' and s(c) =  c - c' are selection coefficients, and g(r), g(sigma), g(c) are invasibility  coefficients (' refers to the mutant traits), which are positive  and do not depend on p. In particular, increased reproduction variance  is always deleterious. We prove that in all three models g(sigma)  = 1/sigma and g(r) = z/sigma for small initial population sizes z.  In model II, g(r) = z/sigma for all z, and we display invasion isoclines  of the 'mean vs variance' type. A slight departure from the isocline  is shown to be more beneficial to alleles with low u than with high  r. In model III, g(c) increases with z like ln(z)/c, and g(r)(Z)  converges to a finite limit L > K/sigma, where K = r/c is the carrying  capacity. For r > 0 the growth invasibility is above z/sigma when  z < K, and below z/sigma when z > K, showing that classical models  I and II underestimate the fixation probabilities in growing populations,  and overestimate them in declining populations. (c) 2006 Elsevier  Inc. All rights reserved.},  Author = {Lambert, A},  Date-Added = {2008-03-28 15:44:55 +1300},  Date-Modified = {2008-03-28 15:45:00 +1300},  Doi = {DOI 10.1016/j.tpb.2006.01.002},  Journal = {Theoretical Population Biology},  Keywords = {continuous-state branching process; diffusion theory; fixation probability; demographic stochasticity; mutant allele; mean-variance trade-off; weak selection},  Pages = {419-441},  Timescited = {0},  Title = {Probability of fixation under weak selection: A branching process unifying approach},  Volume = {69},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tpb.2006.01.002}}  @article{Lambert2005,  Abstract = {In order to model random density-dependence in population dynamics,  we construct the random analogue of the well-known logistic process  in the branching process' framework. This density-dependence corresponds  to intraspecific competition pressure, which is ubiquitous in ecology,  and translates mathematically into a quadratic death rate. The logistic  branching process, or LB-process, can thus be seen as (the mass of)  a fragmentation process (corresponding to the branching mechanism)  combined with constant coagulation rate (the death rate is proportional  to the number of possible coalescing pairs). In the continuous state-space  setting, the LB-process is a time-changed (in Lamperti's fashion)  Ornstein-Uhlenbeck type process. We obtain similar results for both  constructions: when natural deaths do not occur, the LB-process converges  to a specified distribution; otherwise, it goes extinct a.s. In the  latter case, we provide the expectation and the Laplace transform  of the absorption time, as a functional of the solution of a Riccati  differential equation. We also show that the quadratic regulatory  term allows the LB-process to start at infinity, despite the fact  that births occur infinitely often as the initial state goes to \&INFIN;.  This result can be viewed as an extension of the pure-death process  starting from infinity associated to Kingman's coalescent, when some  independent fragmentation is added.},  Author = {Lambert, A},  Date-Added = {2008-03-28 15:43:33 +1300},  Date-Modified = {2008-03-28 15:44:07 +1300},  Journal = {Annals of Applied Probability},  Keywords = {stochastic logistic; size-dependent branching process; continuous-state branching process; population dynamics; logistic process; density dependence; Ornstein-Uhlenbeck type process; Riccati differential equation; fragmentation-coalescence process},  Pages = {1506-1535},  Timescited = {0},  Title = {The branching process with logistic growth},  Volume = {15},  Year = {2005}}  @article{Lanave2000,  Author = {Lanave, C. and Liuni, S. and Licciulli, F. and Attimonelli, M.},  Journal = {Nucleic Acids Research},  Pages = {153--154},  Title = {Update of AMmtDB: a databsae of multi-aligned Metazoa mitochondrial DNA sequences},  Volume = {28},  Year = {2000}}  @article{Lanave1984,  Author = {Lanave, C. and Preparata, G. and Saccone, C. and Serio, G.},  Journal = {Journal of Molecular Evolution},  Pages = {86--93},  Title = {A new method for calculating evolutionary substitution rates},  Volume = {20},  Year = {1984}}  @article{Lanciotti1997,  Author = {Lanciotti, R.S. and Gubler, D.J. and Trent, D.W.},  Journal = {Journal of General Virology},  Notes = {molecular clock},  Pages = {2279--2286},  Title = {Molecular evolution and phylogeny of dengue-4 viruses},  Volume = {78},  Year = {1997}}  @article{Lande1993,  Abstract = {Stochastic factors affecting the demography of a single population  are analyzed to determine the relative risks of extinction from demographic  stochasticity, environmental stochasticity, and random catastrophes.  Relative risks are assessed by comparing asymptotic scaling relationships  describing how the average time to extinction, T, increases with  the carrying capacity of a population, K, under each stochastic factor  alone. Stochastic factors are added to a simple model of exponential  growth up to K. A critical parameter affecting the extinction dynamics  is r, the long-run growth rate of a population below K, including  stochastic factors. If r is positive, with demographic stochasticity  T increases asymptotically as a nearly exponential function of K,  and with either environmental stochasticity or random catastrophes  T increases asymptotically as a power of K. If r is negative, under  any stochastic demographic factor, T increases asymptotically with  the logarithm of K. Thus, for sufficiently large populations, the  risk of extinction from demographic stochasticity is less important  than that from either environmental stochasticity or random catastrophes.  The relative risks of extinction from environmental stochasticity  and random catastrophes depend on the mean and environmental variance  of population growth rate, and the magnitude and frequency of catastrophes.  Contrary to previous assertions in the literature, a population of  modest size subject to environmental stochasticity or random catastrophes  can persist for a long time, if r is substantially positive.},  Author = {Lande, R},  Date-Added = {2008-03-28 15:41:38 +1300},  Date-Modified = {2008-05-23 11:10:25 +1200},  Journal = {American Naturalist},  Pages = {911-927},  Timescited = {0},  Title = {Risks of Population Extinction from Demographic and Environmental Stochasticity and Random Catastrophes},  Volume = {142},  Year = {1993}}  @article{Lang2004,  Author = {Lang, S. and Brezger, A.},  Journal = {Journal of Computational and Graphical Statistics},  Pages = {183--212},  Title = {Bayesian P-splines},  Volume = {13},  Year = {2004}}  @book{Lange2003,  Address = {New York},  Author = {Lange, K.},  Publisher = {Springer},  Series = {Springer Texts in Statistics},  Title = {Applied Probability},  Year = {2003}}  @book{Lange1999,  Address = {New York},  Author = {Lange, K.},  Publisher = {Springer},  Title = {Numerical Analysis for Statisticians},  Year = {1999}}  @book{Lange1997,  Address = {New York},  Author = {Lange, K.},  Publisher = {Springer},  Title = {Mathematical and Statistical Methods for Genetic Analysis},  Year = {1997}}  @article{Lapointe1992,  Author = {Lapointe, F.J. and Legendre, P.},  Journal = {Systematic Biology},  Pages = {158--171},  Title = {A statistical framework to test the consensus among additive trees (cladograms)},  Volume = {41},  Year = {1992}}  @article{Larder1995,  Author = {Larder, B.},  Journal = aidshr,  Notes = {cr},  Pages = {S28--S33},  Title = {Viral Resistance and the selection of anti-retroviral mutants},  Volume = {10},  Year = {1995}}  @article{Larget1999,  Author = {Larget, B. and Simon, D.L.},  Journal = {Molecular Biology and Evolution},  Pages = {750--759},  Title = {Markov chain Monte Carlo algorithms for the Bayesian analysis of phylogenetic trees},  Volume = {16},  Year = {1999}}  @article{Laroche1999,  Author = {Laroche, J. and Bousquet, J.},  Journal = {Molecular Biology and Evolution},  Notes = {indel},  Pages = {441--452},  Title = {Evolution of mitochondrial \textit{rps3} intron in perennial and annual angiosperms and homology to \textit{nad5} intron 1},  Volume = {16},  Year = {1999}}  @article{Lartillot2006,  Author = {Lartillot, N. and Philippe, H.},  Journal = {Systematic Biology},  Pages = {195--207},  Title = {Computing Bayes factors using thermodynamic integration},  Volume = {55},  Year = {2006}}  @article{Laud1995,  Author = {Laud, P.W. and Ibrahim, J.},  Journal = {Journal of the Royal Statistical Society, Series B},  Pages = {247--262},  Title = {Predictive model selection},  Volume = {57},  Year = {1995}}  @techreport{Lavine1997,  Author = {Lavine, M. and Schervish, M.J.},  Institution = {ISDS, Duke University},  Title = {Bayes factors: what they are and what they are not},  Year = {1997}}  @article{Lavine1992,  Author = {Lavine, M. and West, M.},  Journal = {Canadian Journal of Statistics},  Pages = {451--461},  Title = {A Bayesian method for classification and discrimination},  Volume = {20},  Year = {1992}}  @article{Lawrence1993,  Author = {Lawrence, C.E. and Altschul, S.F. and Boguski, M.S. and Liu, J.S. and Neuwald, A.F. and Wootton, J.C.},  Journal = {Science},  Notes = {alignment},  Pages = {208--214},  Title = {Detecting subtle sequence signals: a Gibbs sampling strategy for multiple alignment},  Volume = {262},  Year = {1993}}  @article{Lawrence1999,  Author = {Lawrence, J.G.},  Journal = {Current Opinions in Microbiology},  Notes = {HGT},  Pages = {519--523},  Title = {Gene transfer, speciation and the evolution of bacterial genomes},  Volume = {2},  Year = {1999}}  @article{Lawrence2003,  Author = {Lawrence, J. and Mayers, D.L. and Hullsiek, K.H. and Collins, G. and Abrams, D.I. and Reisler, R.B. and Crane, L.R. and Schmetter, B.S. and Dionne, T.J. and Saldanha, J.M. and Jones, M.C. and Baxter, J.D and of the Terry Beirn Community Programs for Clinical Research on AIDS, 064 Study Team},  Journal = {New England Journal of Medicine},  Pages = {837--846},  Title = {Structured treatment interruption in patients with multidrug-resistant human immunodeficiency virus},  Volume = {28},  Year = {2003}}  @article{Lawrence1998,  Author = {Lawrence, J.G. and Ochman, H.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Notes = {HGT},  Pages = {9413--9417},  Title = {Molecular archaeology of the Escherichia coli genome},  Volume = {95},  Year = {1998}}  @article{Lawrence1997,  Author = {Lawrence, J.G. and Ochman, H.},  Journal = {Journal of Molecular Evolution},  Notes = {HGT},  Pages = {383--397},  Title = {Amelioration of bacterial genomes: rates of change and exchange},  Volume = {44},  Year = {1997}}  @article{Le1991,  Author = {Le, S.Y. and Shapiro, B.A. and Chen, J.H. and Nussinov, R. and Maizel, J.V.},  Journal = {Genetic Analysis Techniques and Applications},  Pages = {191-205},  Title = {RNA pseudoknots downstream of the frameshift sites of retroviruses},  Volume = {8},  Year = {1991}}  @article{Lee2002,  Author = {Lee, T.I. and Rinaldi, N.J. and Robert, F. and Odom, D.T. and Bar-Joseph, Z. and Gerber, G.K. and Hannett, N.M and Harbison, C.T. and Thompson, C.M. and Simon, I. and Zeitlinger, J. and Jennings, E.G. and Murray, H.L. and Gordon, D.B. and Ren, B. and Wyrick, J.J. and Tagne, J.B. and Volkert, T.L. and Fraenkel, E. and Gifford, D.K. and Young, R.A.},  Journal = {Science},  Notes = {networks},  Pages = {799--804},  Title = {Transcriptional regulatory networks in Saccharomyces cerevisiae},  Volume = {298},  Year = {2002}}  @article{Leitner1996,  Author = {Leitner, T. and Escanilla, D. and Franz{\'e}n, C. and Uhl{\'e}n, M. and Albert, J.},  Journal = {Proceedings of the National Academy of Sciences of the United States of America},  Pages = {10864--10869},  Title = {Accurate reconstruction of a known HIV-1 transmission history by phylogenetic tree analysis},  Volume = {93},  Year = {1996}}  @article{Leitner1997a,  Author = {Leitner, T. and Kumar, S. and Albert, J.},  Journal = {Journal of Virology},  Pages = {4761--4770},  Title = {Tempo and mode of nucleotide substitutions in \textit{gag} and \textit{env} gene fragments in human immunodeficieny virus type 1 populations with a known transmission history},  Volume = {71},  Year = {1997}}  @article{Lepage2007,  Author = {Lepage, Thomas and Bryant, David and Philippe, Herve and Lartillot, Nicolas},  Doi = {10.1093/molbev/msm193},  Eprint = {http://mbe.oxfordjournals.org/cgi/reprint/24/12/2669.pdf},  Journal = {Mol Biol Evol},  Number = {12},  Pages = {2669-2680},  Title = {A General Comparison of Relaxed Molecular Clock Models},  Url = {http://mbe.oxfordjournals.org/cgi/content/abstract/24/12/2669},  Volume = {24},  Year = {2007},  Bdsk-Url-1 = {http://mbe.oxfordjournals.org/cgi/content/abstract/24/12/2669},  Bdsk-Url-2 = {http://dx.doi.org/10.1093/molbev/msm193}}  @article{Leroux2001,  Author = {Leroux, C. and Craigo, J.K. and Issel, C.J. and Montelaro, R.C.},  Journal = {Journal of Virology},  Number = {10},  Pages = {4570--4583},  Title = {Equine infectious anemia virus genomic evolution in progressor and nonprogressor ponies},  Volume = {75},  Year = {2001}}  @article{Leroux1997,  Author = {Leroux, C. and Issel, C.J. and Montelaro, R.C.},  Journal = {Journal of Virology},  Keywords = {EIAV; env; rev; LTR; febrile episode; EIAV(PV); quasispecies; principal neutralizing domain; gp90; in vitro fitness; chimeric clone},  Number = {12},  Pages = {9627-39.},  Title = {Novel and dynamic evolution of equine infectious anemia virus genomic quasispecies associated with sequential disease cycles in an experimentally infected pony},  Volume = {71},  Year = {1997}}  @article{Levine2003,  Author = {Levine, R.A. and Yu, Z. and Hanley, W.G. and Nitao, J.J.},  Journal = {Computational Statistics and Data Analysis},  Title = {Implementing componentwise Hastings algorithms},  Volume = {submitted},  Year = {2003}}  @article{Levy2004,  Author = {Levy, D.N. and Aldrovandi, G.M. and Kutsch, O. and Shaw, G.M.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {4204--4209},  Title = {Dynamics of HIV-1 recombination in its natural target cells},  Volume = {101},  Year = {2004}}  @article{Li1999,  Author = {Li, H.C. and Fujiyoshi, T. and Lou, H. and Yashiki, S. and Sonoda, S. and Cartier, L. and Nunez, L. and Munoz, I. and Horai, S. and Tajima, K.},  Journal = {Nature Medicine},  Keywords = {ancient DNA},  Pages = {1428--1432},  Title = {The presence of ancient human T-cell lymphotropic virus type I provirus DNA in an Andea mummy},  Volume = {5},  Year = {1999}}  @article{Li2000,  Author = {Li, S. and Pearl, D. and Doss, H.},  Journal = {Journal of the American Statistical Association},  Pages = {493--508},  Title = {Phylogenetic tree construction using Markov chain Monte Carlo},  Volume = {95},  Year = {2000}}  @article{Li1988,  Author = {Li, W.H. and Tanimura, M. and Sharp, P.M.},  Journal = {Molecular Biology and Evolution},  Pages = {313--330},  Title = {Rates and dates of divergence between AIDS virus nucleotide sequences},  Volume = {5},  Year = {1988}}  @article{Li2001,  Author = {Li, Y. and Carpenter, S.},  Journal = {Journal of General Virology},  Title = {Cis-acting sequences may contribute to size variation in the surface glycoprotein of bovine immunodeficiency virus},  Volume = {in press},  Year = {2001}}  @article{Liangrevisedandresubmitted,  Author = {Liang, L.J. and Weiss, R.E.},  Journal = {Biometrics},  Title = {Importance re-weighting within Gibbs for large data analyses with applications to Bayesian phylogenetic analyses},  Year = {revised and resubmitted}}  @article{Liao2000,  Author = {Liao, D.},  Journal = {Journal of Molecular Evolution},  Notes = {gene conversion},  Pages = {305--317},  Title = {Gene conversion drives within genic sequences: concerted evolution of the ribosomal RNA genes in bacteria and archaea},  Volume = {51},  Year = {2000}}  @article{Liitsola1998,  Author = {Liitsola, K. and Tashkinova, I. and Laukkanen, T. and Korovina, G. and Smolskaja, T. and Momot, O. and Mashkilleyson, N. and Chaplinskas, S. and Brummer-Korvenkontio, H. and Vanhatalo, J. and Leinikki, P. and Salminen, M.O.},  Journal = {AIDS},  Pages = {1907--1919},  Title = {HIV-1 genetic subtype A/B recombinant strain causing an explosive epidemic in injecting drug users in Kaliningrad},  Volume = {12},  Year = {1998}}  @article{Lin1985,  Author = {Lin, S.P. and Bendel, R.B.},  Journal = {Applied Statistics},  Pages = {193--198},  Title = {Algorithm AS 213. Generation of population correlation matrices with specified eigenvalues},  Volume = {34},  Year = {1985}}  @article{Lio1998,  Author = {Lio, P. and Goldman, N.},  Journal = {Genome Research},  Pages = {1233--1244},  Title = {Models of molecular evolution and phylogeny},  Volume = {8},  Year = {1998}}  @book{Liu2001,  Address = {New York, NY},  Author = {Liu, J.S.},  Publisher = {Springer},  Title = {Monte Carlo Strategies in Scientific Computing},  Year = {2001}}  @article{Liu1994,  Author = {Liu, J.S.},  Journal = {Journal of the American Statistical Association},  Notes = {alignment},  Pages = {958--966},  Title = {The collasped Gibbs sampler in Bayesian computations with applications to a gene regulation problem},  Volume = {89},  Year = {1994}}  @article{Liu1999,  Author = {Liu, J.S. and Lawrence, C.E.},  Journal = {Bioinformatics},  Pages = {38--52},  Title = {Bayesian inference on biopolymer models},  Volume = {15},  Year = {1999}}  @techreport{Liu1998,  Author = {Liu, J.S. and Lawrence, C.E.},  Title = {Bayesian inference on biopolymer models},  Year = {1998}}  @article{Liu1995,  Author = {Liu, J.S. and Neuwald, A.F. and Lawrence, C.E.},  Journal = {Journal of the American Statistical Association},  Notes = {alignment},  Pages = {1156--1170},  Title = {Bayesian models for multiple local sequence alignment and Gibbs sampling strategies},  Volume = {90},  Year = {1995}}  @conference{Liu2006,  Address = {,\ Seattle, WA},  Author = {Liu, L. and Pearl, D.K.},  Booktitle = {Joint Statistical Meetings},  Month = {August},  Title = {Reconstructing posterior distributions of a species phylogeny using estimated gene tree distributions},  Year = {2006}}  @article{Liu1997,  Author = {Liu, S.L. and Schacker, T. and Musey, L. and Shriner, D. and McElrath, M.J. and Corey, L. and Mullins, J.I.},  Journal = jv,  Notes = {cr},  Pages = {4284--4295},  Title = {Divergent patterns of progression to AIDS after infection from the same source: Human immunodeficiency virus type 1 evolution and antiviral response},  Volume = {71},  Year = {1997}}  @article{Lloyd2004,  Abstract = {The major role played by demographic stochasticity in determining  the dynamics and persistence of childhood diseases, such as measles,  chickenpox and pertussis, has long been realized. Techniques which  can be used to estimate the magnitude of this stochastic effect are  of clear importance. In this study, we assess and compare the use  of two moment closure approximations to estimate the variability  seen about the average behavior of stochastic models for the recurrent  epidemics seen in childhood diseases. The performance of the approximations  are assessed using analytic techniques available for the simplest  epidemiological model and using numerical simulations in more complex  settings. We also present epidemiologically important extensions  of previous work, considering variability in the SEIR model and in  situations for which there is seasonal variation in disease transmission.  Important implications of stochastic effects for the dynamics of  childhood diseases are highlighted, including serious deficiencies  of deterministic descriptions of dynamical behavior.},  Address = {Program in Theoretical Biology, Institute for Advanced Study, Einstein Drive, Princeton, NJ 08540, USA. [email protected]},  Au = {Lloyd, AL},  Author = {Lloyd, Alun L},  Da = {20031203},  Date-Added = {2008-04-13 17:32:20 +1200},  Date-Modified = {2008-04-13 17:34:46 +1200},  Dcom = {20040310},  Edat = {2003/12/04 05:00},  Issn = {0040-5809 (Print)},  Jid = {0256422},  Journal = {Theor Popul Biol},  Jt = {Theoretical population biology},  Language = {eng},  Lr = {20061115},  Mh = {Demography; *Disease Outbreaks; Humans; *Models, Theoretical; *Population Dynamics; Recurrence; Seasons; Stochastic Processes},  Mhda = {2004/03/11 05:00},  Number = {1},  Own = {NLM},  Pages = {49--65},  Pii = {S0040580903001175},  Pl = {United States},  Pmid = {14642344},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Sb = {IM},  So = {Theor Popul Biol. 2004 Feb;65(1):49-65.},  Stat = {MEDLINE},  Title = {Estimating variability in models for recurrent epidemics: assessing the use of moment closure techniques.},  Volume = {65},  Year = {2004}}  @article{Loftsgaarden1965,  Author = {Loftsgaarden, D.O. and Quesenberry, C.P.},  Journal = {The Annals of Mathematical Statistics},  Pages = {1049--1051},  Title = {A nonparametric estimate of a multivariate density function},  Volume = {36},  Year = {1965}}  @article{Lopes2004,  Author = {Lopes, H.F. and West, M.},  Journal = {Statistica Sinica},  Pages = {41--67},  Title = {Bayesian model assessment in factor analysis},  Volume = {14},  Year = {2004}}  @article{Lopez1999,  Author = {Lopez, F.A. and Manglicmot, J. and Schmidt, T.M. and Yeh, C. and Smith, H.V.},  Journal = {The Journal of Infectious Diseases},  Notes = {id},  Pages = {670--676},  Title = {Molecular characterization of \textit{Cylospora}-like organisms from baboons},  Volume = {179},  Year = {1999}}  @article{loreille2001,  Author = {Loreille, O. and Orlando, L. and Patou-Mathis, M. and Philippe, M. and Taberlet, P. and H{\"a}nni, C.},  Date-Modified = {2012-05-20 11:53:04 +1200},  Journal = {Current Biology},  Number = {3},  Pages = {200--203},  Publisher = {Elsevier},  Title = {{Ancient DNA analysis reveals divergence of the cave bear, Ursus spelaeus, and brown bear, Ursus arctos, lineages}},  Volume = {11},  Year = {2001}}  @article{Lotka1920,  Author = {Lotka, A.J.},  Date-Added = {2008-03-28 16:14:48 +1300},  Date-Modified = {2008-03-28 16:16:12 +1300},  Journal = {J. Am. Chem. Soc.},  Pages = {1595-1599},  Title = {Undamped Oscillations Derived from the Law of Mass Action},  Volume = {42},  Year = {1920}}  @article{Luan2003,  Author = {Luan, Y. and Li, H.},  Journal = {Bioinformatics},  Notes = {expression},  Pages = {474-482},  Title = {Clustering of time-course gene expression using a mixed-effects model with B-splines},  Volume = {19},  Year = {2003}}  @article{Lunter2002,  Author = {Lunter, G. A. and Miklos, I. and Song, Y. S. and Hein, J.},  Journal = {Journal of Computional Biology},  Month = {December},  Number = {6},  Pages = {869--889},  Title = {An efficient algorithm for statistical multiple alignment on arbitrary phylogenetic trees},  Volume = {10},  Year = {2002}}  @article{Lunter2005,  Author = {Lunter, G. and Miklos, I. and Drummond, A. J. and Jensen, J. L. and Hein, J.},  Date-Modified = {2014-07-06 00:53:38 +0000},  Journal = {BMC Bioinformatics},  Pages = {83},  Title = {Bayesian coestimation of phylogeny and sequence alignment},  Volume = {6},  Year = {2005}}  @article{Lunter2003,  Author = {Lunter, G. and Miklos, I. and Drummond, A. J. and Jensen, J. and Hein, J.},  Date-Modified = {2014-07-06 00:53:13 +0000},  Journal = {Lecture Notes in Bioinformatics},  Pages = {228-244},  Title = {Bayesian phylogenetic inference under a statistical indel model},  Volume = {2812},  Year = {2003}}  @article{Lunter2006,  Author = {Lunter, G. and Ponting, C.P. and Hein, J.},  Journal = {PLoS Computational Biology},  Pages = {e5},  Title = {Genome-wide identification of human functional DNA using a neutral indel model},  Volume = {2},  Year = {2006}}  @article{Lutzoni2001,  Author = {Lutzoni, F. and Pagel, M. D. and Peeb, V.},  Date-Modified = {2014-07-06 05:57:27 +0000},  Journal = {Nature},  Pages = {937--940},  Title = {Major fungal lineages are derived from lichen symbiotic ancestors},  Volume = {411},  Year = {2001}}  @article{Lutzoni2000,  Author = {Lutzoni, F. and Wagner, P. and Reeb, V. and Zoller, S.},  Journal = {Systematic Biology},  Notes = {alignment},  Pages = {628--651},  Title = {Integrating ambiguously aligned regions of DNA sequences in phylogentic analyses without violating positional homology},  Volume = {49},  Year = {2000}}  @article{Lyons2000,  Author = {Lyons, T.J. and Gasch, A.P. and Gaither, L.A. and Botstein, D. and Brown, P.O. and Eide, D.J.},  Journal = {Proceedings of the National Academies of Science, USA},  Notes = {yeast expression},  Pages = {7957--7962},  Title = {Genome-wide characterization of the Zap1p zinc-responsive regulon in yeast},  Volume = {97},  Year = {2000}}  @article{Macaulay1999,  Author = {Macaulay, V. and Richards, M. and Sykes, B.},  Journal = {Proceedings of the Royal Society of London, B},  Pages = {2037--2039},  Title = {Mitochondrial DNA recombination -- no need to panic},  Volume = {266},  Year = {1999}}  @article{MacEachern1998,  Author = {MacEachern, S.N. and Muller, P.},  Journal = {Journal of Computational and Graphical Statistics},  Pages = {223--238},  Title = {Estimating mixture of Dirichlet process models},  Volume = {7},  Year = {1998}}  @article{MacNab2003,  Author = {MacNab, Y.C.},  Journal = {Biometrics},  Notes = {spatial},  Pages = {305--316},  Title = {Hierarchical Bayesian modeling of spatially correlated health service outcomes and utilization rates},  Volume = {59},  Year = {2003}}  @article{Maddison1997,  Author = {Maddison, W. P.},  Date-Modified = {2014-07-06 05:56:06 +0000},  Journal = {Systematic Biology},  Notes = {HGT},  Pages = {523--536},  Title = {Gene trees in species trees},  Volume = {46},  Year = {1997}}  @article{Madigan1994,  Author = {Madigan, D. and Raftery, A. E.},  Date-Modified = {2014-12-04 01:10:47 +0000},  Journal = {Journal of the American Statisical Association},  Notes = {model selection},  Pages = {1535--1546},  Title = {Model selection and accounting for model uncertainity in graphical models using Occam Window},  Volume = {89},  Year = {1994}}  @article{Magiorkinis2003,  Author = {Magiorkinis, G. and Paraskevis, D. and Vandamme, A. and Magiorkinis, E. and Sypsa, V. and Hatzakis, A.},  Journal = {Journal of General Virology},  Pages = {2715-2722},  Title = {\textit{In vivo} characteristics of human immunodeficiency virus type 1 intersubtype recombination: determination of hot spots and correlation with sequence similarity},  Volume = {84},  Year = {2003}}  @article{Maidak2000,  Author = {Maidak, B.L. and Cole, J.R. and Lilburn, T.G. and C.T. Parker, Jr. and Saxman, P.R. and Stredwick, J.M. and Garrity, G.M. and Li, B. and Olsen, G.J. and Pramanik, S. and Schmidt, T.M. and Tiedje, J.M.},  Journal = {Nucleic Acids Research},  Pages = {173--174},  Title = {The RDP (Ribosomal Database Project) continues},  Volume = {28},  Year = {2000}}  @article{Makalowski2001,  Author = {Makalowski, W.},  Journal = {Genome Research},  Notes = {tetralogy},  Pages = {667--670},  Title = {Are we polyploids? A brief history of one hypothesis},  Volume = {11},  Year = {2001}}  @article{Malim2001,  Author = {Malim, M. and Emerman, M.},  Journal = {Cell},  Pages = {469--472},  Title = {HIV-1 sequence variation: drift, shift and attenuation},  Volume = {104},  Year = {2001}}  @article{Mallows1973,  Author = {Mallows, C.L.},  Journal = {Technometrics},  Pages = {661--676},  Title = {Some comments on $C_p$},  Volume = {15},  Year = {1973}}  @book{Malthus1798,  Address = {London},  Author = {Malthus, T.R.},  Date-Added = {2008-03-28 16:05:20 +1300},  Date-Modified = {2008-03-28 16:06:35 +1300},  Publisher = {J. Johnson},  Title = {An Essay on the Principle of Population},  Year = {1798}}  @article{Mantzoros2001,  Author = {Mantzoros, C. S. and Ozata, M. and Negrao, A. B. and Suchard, M. A. and Ziotopoulou, M. and Caglayan, S.},  Date-Modified = {2014-07-06 02:08:04 +0000},  Journal = {Journal of Clinical Endocrinology and Metabolism},  Pages = {3284--3291},  Title = {Synchronicity of frequently sampled thyrotropin (TSH) and leptin concentrations in healthy adults and leptin deficient subjects: evidence for possible partial TSH regulation by leptin in humans},  Volume = {86},  Year = {2001}}  @article{Marden2000,  Author = {Marden, J.I.},  Journal = {Journal of the American Statistical Association},  Pages = {1316--1320},  Title = {Hypothesis testing: from $p$ values to Bayes factors},  Volume = {95},  Year = {2000}}  @book{Margulis1981,  Address = {San Francisco},  Author = {Margulis, L.},  Publisher = {W. H. Freeman},  Title = {Symbiosis in Cell Evolution: Life and its Environment on the Early Earth},  Year = {1981}}  @article{Marshall1997,  Author = {Marshall, C.R.},  Journal = {Computing Science and Statistics},  Pages = {218--226},  Title = {Statistical and computational problems in reconstructing evolutionary histories from DNA data},  Volume = {29},  Year = {1997}}  @article{Martin2001,  Author = {Martin, A.},  Journal = {Molecular Biology and Evolution},  Notes = {tetralogy},  Pages = {89--93},  Title = {Is tetralogy true? Lack of support for the one-to-four rule},  Volume = {18},  Year = {2001}}  @article{Martin1999,  Author = {Martin, A.P.},  Journal = {The American Naturalist},  Notes = {tetralogy},  Pages = {111--128},  Title = {Increasing genomic complexity by gene duplication and the origin of vertebrates},  Volume = {154},  Year = {1999}}  @article{Martin1999a,  Author = {Martin, W.},  Journal = {BioEssays},  Notes = {HGT},  Pages = {99--104},  Title = {Mosaic bacterial chromosomes: a challenge en route to a tree of genomes},  Volume = {21},  Year = {1999}}  @article{Martins2002,  Author = {Martins, E.P. and Housworth, E.A.},  Journal = {Systematic Biology},  Notes = {expression; comparative},  Pages = {873--880},  Title = {Phylogeny shape and the phylogenetic comparative method},  Volume = {51},  Year = {2002}}  @article{Mas2000,  Author = {Mas, A. and Parera, M. and Briones, C. and Soriano, V. and Martinez, M.A. and Domingo, E. and Menendez-Arias, L.},  Journal = embo,  Notes = {cr},  Number = {21},  Pages = {5752--5761},  Title = {Role of a dipeptide insertion between codons 69 and 70 of HIV-1 reverse transcriptase and AZT resistance},  Volume = {19},  Year = {2000}}  @article{Matis2004,  Abstract = {This paper develops a stochastic logistic population growth model  with immigration and multiple births. The differential equations  for the low-order cumulant functions (i.e., mean, variance, and skewness)  of the single birth model are reviewed, and the corresponding equations  for the multiple birth model are derived. Accurate approximate solutions  for the cumulant functions are obtained using moment closure methods  for two families of model parameterizations, one for badger and the  other for fox population growth. For both model families, the equilibrium  size distribution may be approximated well using the Normal approximation,  and even more accurately using the saddlepoint approximation. It  is shown that in comparison with the corresponding single birth model,  the multiple birth mechanism increases the skewness and the variance  of the equilibrium distribution, but slightly reduces its mean. Moreover,  the type of density-dependent population control is shown to influence  the sign of the skewness and the size of the variance.},  Address = {Department of Statistics, Texas A\&M University, 3143 TAMU, College Station, TX 77843-3143, USA. [email protected]},  Au = {Matis, JH and Kiffe, TR},  Author = {Matis, James H and Kiffe, Thomas R},  Da = {20031203},  Date-Added = {2008-03-28 15:35:36 +1300},  Date-Modified = {2008-03-28 15:42:42 +1300},  Dcom = {20040310},  Edat = {2003/12/04 05:00},  Issn = {0040-5809 (Print)},  Jid = {0256422},  Journal = {Theor Popul Biol},  Jt = {Theoretical population biology},  Keywords = {stochastic logistic},  Language = {eng},  Mh = {*Animal Migration; Animals; Carnivora; Foxes; Litter Size; Multiple Birth Offspring/*statistics \& numerical data; *Population Growth; *Stochastic Processes},  Mhda = {2004/03/11 05:00},  Number = {1},  Own = {NLM},  Pages = {89--104},  Pii = {S0040580903001151},  Pl = {United States},  Pmid = {14642347},  Pst = {ppublish},  Pt = {Journal article},  Pubm = {Print},  Sb = {IM},  So = {Theor Popul Biol. 2004 Feb;65(1):89-104.},  Stat = {MEDLINE},  Title = {On stochastic logistic population growth models with immigration and multiple births.},  Volume = {65},  Year = {2004}}  @article{Matis2003,  Author = {Matis, James H and Kiffe, Thomas R and Renshaw, E and Hassan, J},  Date-Added = {2008-03-28 16:28:44 +1300},  Date-Modified = {2008-03-28 16:30:52 +1300},  Journal = {Ecological Modelling},  Pages = {239-248},  Title = {A simple saddlepoint approximation for the equilibrium distribution of the stochastic logistic model of population growth},  Volume = {161},  Year = {2003}}  @article{Matseninpress,  Author = {Matsen, F.A.},  Journal = {Systematic Biology},  Title = {A geometric approach to tree shape statistics},  Year = {in press}}  @techreport{Matsen2006,  Author = {Matsen, F.A.},  Institution = {University of Canterbury},  Title = {Optimization over a class of tree shape statistics},  Year = {2006}}  @article{Mau1997,  Author = {Mau, B. and Newton, M.A.},  Journal = {Journal of Computational and Graphical Statistics},  Pages = {122--131},  Title = {Phylogenetic inference for binary data on dendograms using Markov chain Monte Carlo},  Volume = {6},  Year = {1997}}  @misc{May1976,  Author = {May, RM},  Date-Added = {2008-05-21 13:50:51 +1200},  Date-Modified = {2008-05-21 13:51:51 +1200},  Note = {Nature},  Pages = {459-467},  Title = {Simple mathematical models with very complicated dynamics},  Volume = {261},  Year = {1976}}  @article{Mayer-Hamblett2001,  Author = {Mayer-Hamblett, N. and Self, S.},  Journal = {Biometrics},  Pages = {449--460},  Title = {A regression modelling approach for describing patterns of HIV genetic variation},  Volume = {57},  Year = {2001}}  @article{McCabe1995,  Author = {McCabe, K.M. and Khan, G. and Zhang, Y.H. and Mason, E.O. and McCabe, E.R.},  Journal = {Pediatrics},  Notes = {id},  Pages = {165--169},  Title = {Amplification of bacterial DNA using highly conserved sequences: automated analysis and potential for molecular triage of sepsis},  Volume = {95},  Year = {1995}}  @article{McCabe1999,  Author = {McCabe, K.M. and Zhang, Y.H. and Huang, B.L. and Wagar, E.A. and McCabe, E.R.B.},  Journal = {Molecular Genetics and Metabolism},  Notes = {id},  Pages = {205--211},  Title = {Bacterial species identification after DNA amplification with a universal primer pair},  Volume = {66},  Year = {1999}}  @article{McCaskill1990,  Author = {McCaskill, J.S.},  Journal = {Biopolymers},  Pages = {1105-1119},  Title = {The equilibrium partition function and base pairing binding probabilities for RNA secondary structure},  Volume = {29},  Year = {1990}}  @book{McCullagh1983,  Address = {New York, NY},  Author = {McCullagh, P. and Nelder, J.A.},  Publisher = {Chapman \& Hall},  Series = {Monographs on Statistics and Applied Probability},  Title = {Generalized Linear Models},  Year = {1983}}  @article{McCullers1999,  Author = {McCullers, J.A. and Wang, G.C. and He, S. and Webster, R.G.},  Journal = {Journal of Virology},  Pages = {7343--7348},  Title = {Reassortment and insertion-deletion are strategies for the evolution of influenza B viruses in nature},  Volume = {73},  Year = {1999}}  @article{McCutchan1996,  Author = {McCutchan, F.E. and Salminen, M.O. and Carr, J.K. and Burke, D.S.},  Journal = aids,  Notes = {cr},  Number = {S3},  Pages = {S13--S20},  Title = {HIV-1 genetic diversity},  Volume = {10},  Year = {1996}}  @article{McDonald1973,  Author = {McDonald, G.C. and Schwing, R.C.},  Journal = {Technometrics},  Pages = {463--482},  Title = {Instabilities of regression estimates relating air pollution to mortality},  Volume = {15},  Year = {1973}}  @article{McGuire2001,  Author = {McGuire, G. and Denham, M.C. and Balding, D.J.},  Journal = {Molecular Biology and Evolution},  Notes = {alignment},  Pages = {481--490},  Title = {Models of sequence evolution for DNA sequences containing gaps},  Volume = {18},  Year = {2001}}  @article{McKeating1999,  Author = {McKeating, J.A. and Balfe, P.},  Journal = {Immunology Letters},  Pages = {63--70},  Title = {The role of the viral glycoprotein in HIV-1 persistence},  Volume = {65},  Year = {1999}}  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L. and Rodrigo, A. 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Explicit  approximations of the quasi-stationary distribution and of the expected  time to extinction are presented in each of these regions. The quasi-stationary  distribution is approximately normal, and the time to extinction  is long, in one of these regions. Another region has a short time  to extinction and a quasi-stationary distribution that is approximately  truncated geometric. A third region is a transition region between  these two. Here the time to extinction is moderately long and the  quasi-stationary distribution has a more complicated behaviour. Numerical  illustrations are given. (C) 2001 Academic Press.},  Author = {Nasell, I},  Date-Added = {2008-03-28 15:45:41 +1300},  Date-Modified = {2008-03-28 15:45:44 +1300},  Journal = {Journal of Theoretical Biology},  Pages = {11-27},  Timescited = {0},  Title = {Extinction and quasi-stationarity in the Verhulst logistic model},  Volume = {211},  Year = {2001}}  @article{Nasell1996,  Abstract = {The quasi-stationary distribution of the closed stochastic SIS model  changes drastically as the basic reproduction ratio R(0) passes the  deterministic threshold value 1. Approximations are derived that  describe these changes. The quasi-stationary distribution is approximated  by a geometric distribution (discrete!) for R(0) distinctly below  1 and by a normal distribution (continuous!) for R(0) distinctly  above 1. Uniformity of the approximation with respect to R(0) allows  one to study the transition between these two extreme distributions.  We also study the time to extinction and the invasion and persistence  thresholds of the model.},  Author = {Nasell, I},  Date-Added = {2008-03-28 15:45:59 +1300},  Date-Modified = {2008-03-28 15:46:02 +1300},  Journal = {Advances In Applied Probability},  Keywords = {stochastic logistic model; closed stochastic SIS model; time to extinction; threshold of stochastic model; uniform asymptotic approximation},  Pages = {895-932},  Timescited = {0},  Title = {The quasi-stationary distribution of the closed endemic SIS model},  Volume = {28},  Year = {1996}}  @article{Navidi1993,  Author = {Navidi, W.C. and Churchill, G.A. and von Haeseler, A.},  Journal = {Biometrics},  Pages = {543--55},  Title = {Phylogenetic inference: linear invariants and maximum likelihood},  Volume = {49},  Year = {1993}}  @article{Navidi1991,  Author = {Navidi, W.C. and Churchill, G.A. and von Haeseler, A.},  Journal = {Molecular Biology and Evolution},  Pages = {128--143},  Title = {Methods for inferring phylogenies from nucleic acid sequence data by using maximum likelihood and linear invariants},  Volume = {8},  Year = {1991}}  @article{Negroni2001,  Author = {Negroni, M. and Buc, H.},  Journal = {Annual Review of Genetics},  Pages = {275-302},  Title = {Mechanisms of retroviral recombination},  Volume = {35},  Year = {2001}}  @article{Nekrutenko2000,  Author = {Nekrutenko, A. and Li, W.-H.},  Journal = {Genome Research},  Notes = {cg},  Pages = {1986--1995},  Title = {Assessment of compositional heterogeneity within and between Eukaryotic genomes},  Volume = {10},  Year = {2000}}  @article{nee1995,  Author = {Nee, S. 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The  coefficient of variation in the extinction time V is found to have  a maximum value when the death and birth rates are close in value.  For large habitat size K we find that Vmax is of order K1/4 / M1/2,  which is much larger than unity so long as M is small compared to  K1/2. We also present a study of the SLP using the moment closure  approximation (MCA), and discuss the successes and failures of this  method. Regarding the former, the MCA yields a steady-state distribution  for the population when the death rate is low. Although not correct  for the SLP model, the first three moments of this distribution coincide  with those calculated exactly for an adjusted SLP in which extinction  is forbidden. These exact calculations also pinpoint the breakdown  of the MCA as the death rate is increased.},  Address = {Department of Physics and Astronomy, Arizona State University, P.O. Box 871504, Tempe, AZ 85287, USA. [email protected]},  Au = {Newman, TJ and Ferdy, JB and Quince, C},  Author = {Newman, T J and Ferdy, Jean-Baptiste and Quince, C},  Da = {20040209},  Date-Added = {2008-04-13 23:10:57 +1200},  Date-Modified = {2008-04-13 23:11:02 +1200},  Dcom = {20040715},  Doi = {10.1016/j.tpb.2003.10.003},  Edat = {2004/02/10 05:00},  Issn = {0040-5809 (Print)},  Jid = {0256422},  Journal = {Theor Popul Biol},  Jt = {Theoretical population biology},  Language = {eng},  Lr = {20061115},  Mh = {Animals; Environment; *Evolution; *Logistic Models; *Models, Biological; Mortality; *Population Density; *Population Dynamics; Stochastic Processes; Time Factors},  Mhda = {2004/07/16 05:00},  Number = {2},  Own = {NLM},  Pages = {115--126},  Pii = {S0040580903001461},  Pl = {United States},  Pmid = {14766186},  Pst = {ppublish},  Pt = {Comparative Study; Journal article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Theor Popul Biol. 2004 Mar;65(2):115-26.},  Stat = {MEDLINE},  Title = {Extinction times and moment closure in the stochastic logistic process.},  Volume = {65},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tpb.2003.10.003}}  @incollection{Newton1999,  Address = {Hayward, CA},  Author = {Newton, M.A. and Mau, B. and Larget, B.},  Booktitle = {Statistics in Molecular Biology and Genetics: Selected Proceedings of a 1997 Joint AMS-IMS-SIAM Summer Conference on Statistics in Molecular Biology},  Editor = {Seillier-Moiseiwitsch, F.},  Pages = {143--162},  Publisher = {IMS},  Seriestitle = {Lecture Notes - Monograph Series},  Title = {Markov chain Monte Carlo for the Bayesian analysis of evolutionary trees from aligned molecular sequences},  Volume = {33},  Year = {1999}}  @article{Newton1994,  Author = {Newton, M. 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Series B},  Number = {1},  Pages = {99--138},  Title = {Fractional Bayes Factors for Model Comparison (With Discussion)},  Volume = {57},  Year = {1995}}  @article{Oakley2003,  Author = {Oakley, T.H.},  Journal = {Integrative and Comparative Biology},  Pages = {522--530},  Title = {On homology of arthropod compound eyes},  Volume = {43},  Year = {2003}}  @article{Oakley2003a,  Author = {Oakley, T.H.},  Journal = {Trends in Ecology \& Evolution},  Pages = {623--627},  Title = {The eye as a replicating and diverging, modular development unit},  Volume = {18},  Year = {2003}}  @article{Oakley2002,  Author = {Oakley, T.H. and Cunningham, C.W.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {1426--1430},  Title = {Molecular phylogenetic evidence for the independent evolutionary origin of an arthropod compound eye},  Volume = {99},  Year = {2002}}  @article{Oakley2005,  Author = {Oakley, T.H. and Gu, Z. and Abouheif, E. and Patel, N.H. and Li, W.-H.},  Journal = {Molecular Biology and Evolution},  Notes = {yeast expression, comparative method},  Pages = {40--50},  Title = {Comparative methods for the analysis of gene-expression evolution: an example using yeast functional genomic data},  Volume = {22},  Year = {2005}}  @article{Odell1966,  Author = {Odell, P.L. and Feiveson, A.H.},  Journal = {Journal of the American Statistical Assocation},  Pages = {199--203},  Title = {A numerical procedure to generate a sample covariance matrix},  Volume = {61},  Year = {1966}}  @article{Ogurtsov2004,  Author = {Ogurtsov, A.Y. and Sunyaev, S. and Kondrashov, A.S.},  Journal = {Genome Research},  Notes = {indel},  Pages = {1610--1614},  Title = {Indel-based evolutionary distance and mouse-human divergence},  Volume = {14},  Year = {2004}}  @article{Oh1999,  Author = {Oh, M-S.},  Journal = {Computational Statistics \& Data Analysis},  Pages = {411--427},  Title = {Estimation of posterior density functions from a posterior sample},  Volume = {29},  Year = {1999}}  @article{Olsson2002,  Author = {Olsson, A.Y. and Lundwall, A.},  Journal = {Biochemical and Biophysical Research Communications},  Pages = {305--311},  Title = {Organization and evolution of the glandular kallikrein locus in Mus musculus},  Volume = {299},  Year = {2002}}  @article{Orlando2002,  Author = {Orlando, L. and Bonjean, D. and Bocherens, H. and Thenot, A. and Argant, A. and Otte, M. and H\anni, C.},  Journal = {Molecular Biology and Evolution},  Notes = {serial samples},  Pages = {1920--1933},  Title = {Ancient DNA and the population genetics of cave bears (\textit{Ursus spelaeus}) through space and time},  Volume = {19},  Year = {2002}}  @article{Overbaugh2001,  Author = {Overbaugh, J. and Bangham, C.R.},  Journal = {Science},  Pages = {1106--1109},  Title = {Selection forces and constraints on retroviral sequence variation},  Volume = {292},  Year = {2001}}  @article{Pachter2004,  Author = {Pachter, L. and Sturmfels, B.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {16138--16143},  Title = {Parametric inference for biological sequence analysis},  Volume = {101},  Year = {2004}}  @article{Pachter2004a,  Author = {Pachter, L. and Sturmfels, B.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {16132--16137},  Title = {Tropical geometry of statistical models},  Volume = {101},  Year = {2004}}  @article{Padua2003,  Author = {Padua, E. and Jenkins, A. and Brown, S. and Bootman, J. and Paixao, M.T. and Almond, N. and Berry, N.},  Journal = {Journal of General Virology},  Pages = {1287--1299},  Title = {Natural variation of the \textit{nef} gene in human immunodeficiency virus type-2 infections},  Volume = {84},  Year = {2003}}  @article{Page2000,  Author = {Page, R.D.M.},  Journal = {Molecular Phylogenetics and Evolution},  Pages = {89--106},  Title = {Extracting species trees from complex gene trees: reconciled trees and vertebrate phylogeny},  Volume = {14},  Year = {2000}}  @article{Page1996,  Author = {Page, R.D.M.},  Journal = {Sysmatic Biology},  Pages = {92--98},  Title = {Temporal congruence revisited: comparison of mitochondrial DNA sequence divergence in cospeciating pocket gophers and their chewing live},  Volume = {45},  Year = {1996}}  @article{Pagel1999,  Author = {Pagel, M. D.},  Date-Modified = {2014-07-06 05:57:11 +0000},  Journal = {Systematic Biology},  Pages = {612--622},  Title = {The maximum likelihood approach to reconstructing ancestral character states of discrete characters on phylogenies},  Volume = {48},  Year = {1999}}  @inbook{Pagel2002,  Address = {Berlin},  Author = {Pagel, M. D. and Lutzoni, F.},  Chapter = {Accounting for phylogenetic uncertainty in comparative studies of evolution and adaptation},  Date-Modified = {2014-07-06 06:03:29 +0000},  Pages = {148--161},  Publisher = {Springer-Verlag},  Title = {Biological Evolution and Statistical Physics},  Year = {2002}}  @article{Pagel2004,  Author = {Pagel, M. D. and Meade, A. and Barker, D. M.},  Date-Modified = {2014-07-06 06:03:45 +0000},  Journal = {Systematic Biology},  Pages = {673--684},  Title = {Bayesian estimation of ancestral character states on phylogenies},  Volume = {53},  Year = {2004}}  @article{Palella1998,  Author = {Palella, F.J. and Delaney, K.M. and Moorman, A.C. and Loveless, M.O. and Fuher, J. and Satten, G.A. and Aschman, D.J. and Holmberg, S.D.},  Journal = {New England Journal of Medicine},  Pages = {853--60},  Title = {Declining morbidity and motality among patients with advanced HIV infection},  Volume = {338},  Year = {1998}}  @article{Palella1998a,  Author = {Palella, F.J. and Delaney, K.M. and Moorman, A.C. and Loveless, M.O. and Fuhrer, J. and Satten, G.A. and Aschman, D.J. and Holmberg, S.D.},  Journal = {New England Journal of Medicine},  Pages = {853--860},  Title = {Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators},  Volume = {338},  Year = {1998}}  @article{Pang1997,  Author = {Pang, H. and Kong, X.G. and Sentsui, H. and Kono, Y. and Sugiura, T. and Hasegawa, A. and Akashi, H.},  Journal = {The Journal of Veterinary Medical Science},  Keywords = {EIAV; PND; HVR; P337; Wyoming; insertion/deletion; indel},  Number = {12},  Pages = {1089--1095},  Title = {Genetic variation of envelope gp90 gene of equine infectious anemia virus isolated from an experimentally infected horse},  Volume = {59},  Year = {1997}}  @article{Paradis2003,  Author = {Paradis, E. and Claude, J. and Strimmer, K.},  Journal = {Bioinformatics},  Pages = {289--290},  Title = {APE: analysis of phylogenetics and evolution in R language},  Volume = {20},  Year = {2003}}  @article{Paraskevis2003,  Author = {Paraskevis, D. and Lemey, P. and Salemi, M. and Suchard, M. A. and der Peer, Y. Van and Vandamme, A.},  Date-Modified = {2014-07-06 02:35:36 +0000},  Journal = {Molecular Biology and Evolution},  Pages = {1986--1996},  Title = {Analysis of the evolutionary relationships of HIV-1 and SIVcpz sequences using Bayesian inference: implications for the origins of HIV-1},  Volume = {20},  Year = {2003}}  @article{Parsons2007,  Abstract = {We extend the one-locus two allele Moran model of fixation in a haploid  population to the case where the total size of the population is  not fixed. The model is defined as a two-dimensional birth-and-death  process for allele number. Changes in allele number occur through  density-independent death events and birth events whose per capita  rate decreases linearly with the total population density. Uniquely  for models of this type, the latter is determined by these same birth-and-death  events. This provides a framework for investigating both the effects  of fluctuation in total population number through demographic stochasticity,  and deterministic density-dependent changes in mean density, on allele  fixation. We analyze this model using a combination of asymptotic  analytic approximations supported by numerics. We find that for advantageous  mutants demographic stochasticity of the resident population does  not affect the fixation probability, but that deterministic changes  in total density do. In contrast, for deleterious mutants, the fixation  probability increases with increasing resident population fluctuation  size, but is relatively insensitive to initial density. These phenomena  cannot be described by simply using a harmonic mean effective population  size.},  Address = {Department of Mathematics, University of Toronto, 40 St. George Street, Toronto, Ont., Canada M5S 2E4. [email protected]},  Au = {Parsons, TL and Quince, C},  Author = {Parsons, Todd L and Quince, Christopher},  Da = {20070612},  Date-Added = {2008-04-13 17:20:00 +1200},  Date-Modified = {2008-04-13 17:26:36 +1200},  Dcom = {20071218},  Dep = {20061215},  Doi = {10.1016/j.tpb.2006.11.004},  Edat = {2007/01/24 09:00},  Issn = {0040-5809 (Print)},  Jid = {0256422},  Journal = {Theor Popul Biol},  Jt = {Theoretical population biology},  Language = {eng},  Mh = {Alleles; Genetics, Population/*methods; *Haploidy; Logistic Models; Markov Chains; *Models, Genetic; Mutation/genetics; Population Density; *Stochastic Processes},  Mhda = {2007/12/19 09:00},  Number = {1},  Own = {NLM},  Pages = {121--135},  Pii = {S0040-5809(06)00163-8},  Pl = {United States},  Pmid = {17239910},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Theor Popul Biol. 2007 Aug;72(1):121-35. Epub 2006 Dec 15.},  Stat = {MEDLINE},  Title = {Fixation in haploid populations exhibiting density dependence I: The non-neutral case.},  Volume = {72},  Year = {2007},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.tpb.2006.11.004}}  @article{Patel2001,  Author = {Patel, M. and Dorman, K.S. and Zhang, Y.H. and Huang, B.L. and Arnold, A.P. and Sinsheimer, J.S. and Vilain, E. and McCabe, E.R.B.},  Journal = {American Journal of Human Genetics},  Pages = {275--280},  Title = {Priamte DAX1, SRY and SOX9: evolutionary stratification of sex determination pathway},  Volume = {68},  Year = {2001}}  @article{Pathak1992,  Author = {Pathak, V. and Temin, H.},  Journal = {Journal of Virology},  Pages = {3093--3100},  Title = {5-azacytidine and RNA secondary structure increase the retrovirus mutation rate},  Volume = {66},  Year = {1992}}  @article{Peleg2003,  Author = {Peleg, O. and Trifonov, E.N. and Bolshoy, A.},  Journal = {Nucleic Acids Research},  Pages = {4192-4200},  Title = {Hidden messages in the nef gene of human immunodeficiency virus type 1 suggest a novel RNA secondary structure},  Volume = {31},  Year = {2003}}  @article{Penny1986,  Author = {Penny, D. and Hendy, M.D.},  Journal = {Molecular Biology and Evolution},  Pages = {403--417},  Title = {Estimating the reliability of evolutionary trees},  Volume = {3},  Year = {1986}}  @article{Perez-Hoyos2003,  Author = {Perez-Hoyos, S. and del Amo J, J. and Muga, R. and del Romero, J. and de Olalla, P. Garcia and Guerrero, R. and Hernandez-Aguado, I. and of Seroconverters, Spanish Multicenter Study Group},  Journal = {AIDS},  Pages = {353--359},  Title = {Effectiveness of highly active antiretroviral therapy in Spanish cohorts of HIV seroconverters: differences by transmission category},  Volume = {17},  Year = {2003}}  @article{Peruggia1997,  Author = {Peruggia, M.},  Journal = {Journal of the American Statistical Assocation},  Pages = {199--207},  Title = {On the variability of case-deletion importance sampling weights in the Bayesian linear model},  Volume = {92},  Year = {1997}}  @article{Philpott2005,  Author = {Philpott, S.M. and Burger, H. and Tsoukas, C. and Foley, B. and Anastos, K. and Kitchen, C.M.R. and Weiser, B.},  Journal = {Journal of Virology},  Pages = {353--363},  Title = {Human immunodeficieny virsus type 1 genomic RNA sequences in the female genital tract and blood: compartmentalization and intrapatient recombination},  Volume = {79},  Year = {2005}}  @article{Philpott2001,  Author = {Philpott, S. and Weiser, B. and Anastos, K. and Kitchen, C.M.R. and Robinson, E. and Meyer, W.A. and Sackd, H.S. and S, Philpott and B, Weiser and K, Anastos and CMR, Kitchen and E, Robinson and WA, Meyer and HS, Sackd and MAther-WaghU and C, Brunner and H, Burger and Brunner, C. and Burger, H.},  Journal = jci,  Notes = {cr},  Pages = {431--438},  Title = {Preferential suppression of CXCR4-specific strains of HIV-1 by antiviral therapy},  Volume = {107},  Year = {2001}}  @article{Philpott2001a,  Author = {Philpott, S. and Weiser, B. and Anastos, K. and Kitchen, C.M.R. and Robison, E. and III, W.A. Meyer and Sacks, H.S. and Mathut-Wagh, U. and Brunner, C. and Burger, H.},  Journal = {The Journal of Clinical Investigation},  Notes = {serial},  Pages = {431--438},  Title = {Preferential suppression of CXCR4-specific strains of HIV-1 by antiviral therapy},  Volume = {107},  Year = {2001}}  @article{Pillai2003,  Author = {Pillai, S. and Good, B. and Richman, D. and Corbeil, J.},  Journal = {AIDS Research and Human Retroviruses},  Pages = {145--149},  Title = {A new perspective on V3 phenotype prediction},  Volume = {19},  Year = {2003}}  @article{Pillai2006,  Author = {Pillai, S.K. and Kosakovsky-Pond, S.L. and Liu, Y. and Good, B.M. and Strain, M.C. and Ellis, R.J. and Letendre, S. and Smith, D.M. and Guenthard, H.F. and Grant, I. and Marcotte, T.D. and McCutchan, J.A. and Richmand, D.D. and Wong, J.K.},  Journal = {Brain},  Pages = {1872--1883},  Title = {Genetic attributes of cerebrospinal fluid-derived HIV-1 env},  Volume = {129},  Year = {2006}}  @article{Pinheiro1997,  Author = {Pinheiro, A. and Vidakovic, B.},  Journal = {Computational Statistics \& Data Analysis},  Pages = {399--415},  Title = {Estimating the square root of a density via compactly supported wavelets},  Volume = {25},  Year = {1997}}  @article{Podlaha2005,  Author = {Podlaha, O. and Webb, D.M. and Tucker, P.K. and Zhang, J.},  Journal = {Molecular Biology and Evolution},  Notes = {indel; positive selection},  Pages = {1845--1852},  Title = {Positive selection for indel substitutions in the rodent sperm protein catsper1},  Volume = {22},  Year = {2005}}  @article{Politis1994,  Author = {Politis, D.N. and Romano, J.P.},  Journal = {Journal of the American Statistical Association},  Pages = {1303--1313},  Title = {The stationary bootstrap},  Volume = {89},  Year = {1994}}  @article{Pontiggia1994,  Author = {Pontiggia, A. and Rimini, R. and Harley, V.R. and Goodfellow, P.N. and Lovellbadge, R. and Bianchi, M.E.},  Journal = {EMBO Journal},  Pages = {6115--6124},  Title = {Sex-reversing mutations affect the architecture of SRY-DNA complexes},  Volume = {13},  Year = {1994}}  @article{Porter2003,  Author = {Porter, K. and Babiker, A. and Bhaskaran, K. and Darbyshire, J. and Pezzotti, P. and Porter, K. and Walker, A.S. and Collaboration, CASCADE},  Journal = {Lancet},  Pages = {1267--1274},  Title = {Determinants of survival following HIV-1 seroconversion after the introduction of HAART},  Volume = {362},  Year = {2003}}  @article{Posada2004,  Author = {Posada, D. and Buckley, T.R.},  Journal = {Systematic Biology},  Pages = {793--808},  Title = {Model selection and model averaging in phylogenetics: advantages of Akaike information criterion and Bayesian approaches over likelihood ratio tests},  Volume = {53},  Year = {2004}}  @article{Posada2001,  Author = {Posada, D. and Crandall, K.A.},  Journal = {Molecular Biology and Evolution},  Pages = {897--906},  Title = {Selecting models of nucleotide substitution: an application to human immunodeficiency virus 1 (HIV-1)},  Volume = {18},  Year = {2001}}  @article{Posada2001a,  Author = {Posada, D. and Crandall, K.A.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Pages = {13757--13762},  Title = {Evaluation of methods for detecting recombination from DNA sequences: computer simulations},  Volume = {98},  Year = {2001}}  @book{Press1992,  Address = {Cambridge},  Author = {Press, W.H. and Teukolsky, S.A. and Vetterling, W.T. and Flannery, B.P.},  Edition = {2nd},  Publisher = {Cambridge University Press},  Title = {Numerical Recipes in C: The Art of Scientific Computing},  Year = {1992}}  @article{Pupko2002,  Author = {Pupko, T. and Huchon, D. and Cao, Y. and Okada, N. and Hasegawa, M.},  Journal = {Molecular Biology and Evolution},  Notes = {hierarchical models},  Pages = {2294--2307},  Title = {Combining multiple data sets in a likelihood analysis: which models are the best?},  Volume = {19},  Year = {2002}}  @article{Purvis2002,  Author = {Purvis, A. and Katzourakis, A. and Agapow, P.-M.},  Journal = {Journal of Theoretical Biology},  Notes = {Tree Shape},  Pages = {99--103},  Title = {Evaluating phylogenetic tree shape: two modifications of Fusco \& Cronk's method},  Volume = {214},  Year = {2002}}  @article{Pybus2006,  Author = {Pybus, O.G.},  Journal = {PLoS Biology},  Pages = {e151},  Title = {Model selection and the molecular clock},  Volume = {4},  Year = {2006}}  @article{Pybus2000,  Author = {Pybus, O. G. and Rambaut, A. and Harvey, P. H.},  Date-Modified = {2013-02-13 01:22:22 +0000},  Journal = {Genetics},  Pages = {1429--1437},  Title = {An integrated framework for the inference of viral population history from reconstructed genealogies},  Volume = {155},  Year = {2000}}  @article{Pybus2001,  Abstract = {Hepatitis C virus (HCV) is a leading worldwide cause of liver disease.  Here, we use a new model of HCV spread to investigate the epidemic  behavior of the virus and to estimate its basic reproductive number  from gene sequence data. We find significant differences in epidemic  behavior among HCV subtypes and suggest that these differences are  largely the result of subtype-specific transmission patterns. Our  model builds a bridge between the disciplines of population genetics  and mathematical epidemiology by using pathogen gene sequences to  infer the population dynamic history of an infectious disease.},  Au = {Pybus, OG and Charleston, MA and Gupta, S and Rambaut, A and Holmes, EC and Harvey, PH},  Author = {Pybus, O G and Charleston, M A and Gupta, S and Rambaut, A and Holmes, E C and Harvey, P H},  Da = {20010625},  Date-Added = {2008-04-13 17:01:59 +1200},  Date-Modified = {2014-07-03 23:04:27 +0000},  Dcom = {20010712},  Doi = {10.1126/science.1058321},  Edat = {2001/06/26 10:00},  Issn = {0036-8075 (Print)},  Jid = {0404511},  Journal = {Science},  Jt = {Science (New York, N.Y.)},  Language = {eng},  Lr = {20070319},  Mh = {Endemic Diseases; Epidemiology, Molecular; Genes, Viral; Hepacivirus/classification/genetics/*physiology; Hepatitis C/*epidemiology/transmission/*virology; Humans; Likelihood Functions; Models, Biological; Phylogeny; Population Dynamics; Prevalence; Substance Abuse, Intravenous/complications},  Mhda = {2001/07/13 10:01},  Number = {5525},  Own = {NLM},  Pages = {2323--2325},  Pii = {292/5525/2323},  Pl = {United States},  Pmid = {11423661},  Pst = {ppublish},  Pt = {Journal article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Sb = {IM},  So = {Science. 2001 Jun 22;292(5525):2323-5.},  Stat = {MEDLINE},  Title = {The epidemic behavior of the hepatitis C virus.},  Volume = {292},  Year = {2001},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1058321}}  @article{Qian2001,  Author = {Qian, B. and Goldstein, R.A.},  Journal = {Proteins},  Notes = {indel},  Pages = {102--104},  Title = {Distribution of indel lengths},  Volume = {45},  Year = {2001}}  @other{Queiroz2007,  Author = {de Queiroz, Alan and Gatesy, John},  Issn = {0169-5347},  Month = jan,  Number = {1},  Owner = {dpm},  Pages = {34--41},  Refid = {S0169-5347(06)00332-6 DOI - 10.1016/j.tree.2006.10.002},  Timestamp = {2009.01.25},  Title = {The supermatrix approach to systematics},  Url = {http://linkinghub.elsevier.com/retrieve/pii/S0169534706003326},  Volume = {22},  Year = {2007},  Bdsk-Url-1 = {http://linkinghub.elsevier.com/retrieve/pii/S0169534706003326}}  @article{Racine-Poon1988,  Author = {Racine-Poon, A.},  Journal = {Journal of the American Statistical Assocation},  Notes = {calibration},  Pages = {650--656},  Title = {A Bayesian approach to nonlinear calibration problems},  Volume = {83},  Year = {1988}}  @article{Racine-Poon1991,  Author = {Racine-Poon, A. and Weihs, C. and Smith, A.F.M.},  Journal = {Biometrics},  Notes = {calibration,serial dilution},  Pages = {1235--1246},  Title = {Estimation of relative potency with sequential dilution errors in radioimmunoassay},  Volume = {47},  Year = {1991}}  @incollection{Raftery1996,  Address = {New York, NY},  Author = {Raftery, A. E. and Lewis, S. M.},  Booktitle = {Markov Chain Monte Carlo in Practice},  Date-Modified = {2014-12-04 01:11:07 +0000},  Editor = {Gilks, W.R. and Richardson, S. and Spiegelhalter, D.J.},  Pages = {115--130},  Publisher = {Chapman \& Hall},  Title = {Implementing MCMC},  Year = {1996}}  @techreport{Raftery2006,  Author = {Raftery, A. E. and Newton, M. A. and Satagopan, J. and Krivistsky, P.},  Date-Modified = {2014-12-04 01:11:13 +0000},  Institution = {Department of Statistics, University of Washington},  Number = {499},  Title = {Estimating the integrated likelihood via posterior simulation using the harmonic mean identity},  Year = {2006}}  @article{Ragan2001,  Author = {Ragan, M.A.},  Journal = {Current Opinion in Genetics \& Development},  Notes = {HGT},  Pages = {620--626},  Title = {Detection of lateral gene transfer among microbial genomes},  Volume = {11},  Year = {2001}}  @article{Rambaut2000,  Author = {Rambaut, A.},  Journal = {Bioinformatics},  Notes = {molecular clock},  Pages = {395--399},  Title = {Estimating the rate of molecular evolution: incorporating non-contemporaneous sequences into maximum likelihood phylogenies},  Volume = {16},  Year = {2000}}  @article{Ramoni2002,  Author = {Ramoni, M.F. and Sebastian, P. and Kohane, I.S.},  Journal = {Proceedings of the National Academy of Sciences, USA},  Notes = {expression},  Pages = {9121--9126},  Title = {Cluster analysis of gene expression dynamics},  Volume = {99},  Year = {2002}}  @article{Rannala2007,  Author = {Rannala, Bruce and Yang, Ziheng},  Date-Modified = {2012-05-18 14:56:06 +1200},  Journal = {Systematic Biology},  Number = {3},  Owner = {dpm},  Pages = {453--466},  Publisher = {Taylor \& Francis},  Timestamp = {2008.12.03},  Title = {Inferring Speciation Times under an Episodic Molecular Clock},  Volume = {56},  Year = {2007},  Bdsk-Url-1 = {http://www.informaworld.com/10.1080/10635150701420643}}  @article{Rannala1996,  Author = {Rannala, B. and Yang, Z.},  Journal = {Journal of Molecular Evolution},  Pages = {304--311},  Title = {Probability distribution of molecular evolutionary trees: a new method of phylogenetic inference},  Volume = {43},  Year = {1996}}  @article{Rao1996,  Author = {Rao, C.R. and Dhanbag, D.N.},  Journal = {Proceedings of the American Mathematical Society},  Page = {299-302},  Title = {A note on a characteristic property based on order statistics},  Volume = {124},  Year = {1996}}  @article{Reitz1992,  Author = {Reitz, M.S. and Guo, H.G. and Oleske, J. and Hoxie, J. and Popovic, M. and Read-Connole, E. and Markham, P. and Streicher, H. and Gallo, R.G.},  Journal = {AIDS Research and Human Retroviruses},  Pages = {1539--1541},  Title = {On the historical origins of HIV-1 (MN) and (RF)},  Volume = {8},  Year = {1992}}  @article{Relman1999,  Author = {Relman, D.A.},  Journal = {Science},  Notes = {id},  Pages = {1308--1310},  Title = {The search for unrecognized pathogens},  Volume = {284},  Year = {1999}}  @article{Relman1998,  Author = {Relman, D.A.},  Journal = {Emerging Infectious Diseases},  Notes = {id},  Pages = {382--389},  Title = {Detection and identification of previously unrecognized microbial pathogens},  Volume = {4},  Year = {1998}}  @article{Relman1990,  Author = {Relman, D.A. and Loutit, J.S. and Schmidt, T.M. and Falkow, S. and Tompkin, L.S.},  Journal = {New England Journal of Medicine},  Pages = {1573--1580},  Title = {The agent of bacillary angiomatosis: an approach to the identification of uncultured pathogens},  Volume = {323},  Year = {1990}}  @article{Relman1996,  Author = {Relman, D.A. and Schmidt, T.M. and Gajadhar, A. and Sogin, M. and Cross, J. and Yoder, K. and Sethabutr, O. and Echeverria, P.},  Journal = {Journal of Infectious Diseases},  Notes = {id},  Pages = {440--445},  Title = {Molecular phylogenetic analysis of Cyclospora, the human intestinal pathogen, suggests that it is closely related to Eimeria species},  Volume = {173},  Year = {1996}}  @article{Relman1992,  Author = {Relman, D.A. and Schmidt, T.M. and MacDermott, R.P. and Falkow, S.},  Journal = {New England Journal of Medicine},  Notes = {id},  Pages = {293--301},  Title = {Identification of the uncultered bacillus of Whipple's disease},  Volume = {327},  Year = {1992}}  @article{Ren2008,  Abstract = {Supermatrix and supertree methods are two strategies advocated for  phylogenetic analysis of sequence data from multiple gene loci, especially  when some species are missing at some loci. The supermatrix method  concatenates sequences from multiple genes into a data supermatrix  for phylogenetic analysis, and ignores differences in evolutionary  dynamics among the genes. The supertree method analyzes each gene  separately and assembles the subtrees estimated from individual genes  into a supertree for all species. Most algorithms suggested for supertree  construction lack statistical justifications and ignore uncertainties  in the subtrees. Instead of supermatrix or supertree, we advocate  the use of likelihood function to combine data from multiple genes  while accommodating their differences in the evolutionary process.  This combines the strengths of the supermatrix and supertree methods  while avoiding their drawbacks. We conduct computer simulation to  evaluate the performance of the supermatrix, supertree, and maximum  likelihood methods applied to two phylogenetic problems: molecular-clock  dating of species divergences and reconstruction of species phylogenies.  The results confirm the theoretical superiority of the likelihood  method. Supertree or separate analyses of data of multiple genes  may be useful in revealing the characteristics of the evolutionary  process of multiple gene loci, and the information may be used to  formulate realistic models for combined analysis of all genes by  likelihood.},  Author = {Ren, F. and Tanaka, H. and Yang, Z.},  Citeulike-Article-Id = {3858651},  Doi = {http://dx.doi.org/10.1016/j.gene.2008.04.002},  Issn = {03781119},  Journal = {Gene},  Keywords = {phylogenetics, supermatrix, supertrees},  Month = {April},  Posted-At = {2009-01-07 20:19:46},  Priority = {2},  Title = {A likelihood look at the supermatrix--supertree controversy},  Url = {http://dx.doi.org/10.1016/j.gene.2008.04.002},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.gene.2008.04.002}}  @article{Rest2003,  Author = {Rest, J.S. and Mindell, D.P.},  Journal = {Infection, Genetics and Evolution},  Pages = {219--225},  Title = {SARS associated coronavirus has a recombinant polymerase and coronaviruses have a history of host-shifting},  Volume = {3},  Year = {2003}}  @inbook{Rice2002,  Address = {Baltimore, MD},  Author = {Rice, S.H.},  Booktitle = {Human Evolution through Developmental Change},  Editors = {N. 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There are, however, a growing number of examples in which large Bayesian posterior clade probabilities are associated with very short branch lengths and low values for non-Bayesian measures of support such as nonparametric bootstrapping. For the four-taxon case when the true tree is the star phylogeny, Bayesian analyses become increasingly unpredictable in their preference for one of the three possible resolved tree topologies as data set size increases. This leads to the prediction that hard (or near-hard) polytomies in nature will cause unpredictable behavior in Bayesian analyses, with arbitrary resolutions of the polytomy receiving very high posterior probabilities in some cases. We present a simple solution to this problem involving a reversible-jump Markov chain Monte Carlo (MCMC) algorithm that allows exploration of all of tree space, including unresolved tree topologies with one or more polytomies. The reversible-jump MCMC approach allows prior distributions to place some weight on less-resolved tree topologies, which eliminates misleadingly high posteriors associated with arbitrary resolutions of hard polytomies. Fortunately, assigning some prior probability to polytomous tree topologies does not appear to come with a significant cost in terms of the ability to assess the level of support for edges that do exist in the true tree. Methods are discussed for applying arbitrary prior distributions to tree topologies of varying resolution, and an empirical example showing evidence of polytomies is analyzed and discussed.},  Au = {Lewis, PO and Holder, MT and Holsinger, KE},  Author = {Lewis, Paul O and Holder, Mark T and Holsinger, Kent E},  Da = {20050713},  Date-Added = {2008-11-28 18:55:33 -0800},  Date-Modified = {2014-07-06 00:37:13 +0000},  Dcom = {20050818},  Doi = {10.1080/10635150590924208},  Edat = {2005/07/14 09:00},  Issn = {1063-5157 (Print)},  Jid = {9302532},  Journal = {Syst Biol},  Jt = {Systematic biology},  Language = {eng},  Lr = {20061115},  Mh = {Algae, Green/genetics; *Bayes Theorem; Classification/*methods; *Data Interpretation, Statistical; Markov Chains; Monte Carlo Method; *Phylogeny; Reproducibility of Results},  Mhda = {2005/08/19 09:00},  Number = {2},  Own = {NLM},  Pages = {241--253},  Pii = {X8576658LP734021},  Pl = {England},  Pmid = {16012095},  Pst = {ppublish},  Pt = {Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Syst Biol. 2005 Apr;54(2):241-53.},  Stat = {MEDLINE},  Title = {Polytomies and Bayesian phylogenetic inference.},  Volume = {54},  Year = {2005},  Bdsk-Url-1 = {http://dx.doi.org/10.1080/10635150590924208}}  @article{Thorne:1998lh,  Abstract = {A simple model for the evolution of the rate of molecular evolution is presented. With a Bayesian approach, this model can serve as the basis for estimating dates of important evolutionary events even in the absence of the assumption of constant rates among evolutionary lineages. The method can be used in conjunction with any of the widely used models for nucleotide substitution or amino acid replacement. It is illustrated by analyzing a data set of rbcL protein sequences.},  Address = {Statistics Department, North Carolina State University, Raleigh 27695-8203, USA. [email protected]},  Au = {Thorne, JL and Kishino, H and Painter, IS},  Author = {Thorne, J L and Kishino, H and Painter, I S},  Da = {19990119},  Date-Added = {2008-11-28 18:43:28 -0800},  Date-Modified = {2008-11-28 18:43:28 -0800},  Dcom = {19990119},  Edat = {1998/12/29},  Gr = {P01-GM45344/GM/United States NIGMS},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Lr = {20071114},  Mh = {Algorithms; *Evolution; *Evolution, Molecular; *Models, Genetic; Models, Statistical; *Phylogeny; Plant Proteins/genetics; Plants/*classification/*genetics; *Ribulose-Bisphosphate Carboxylase; *Time},  Mhda = {1998/12/29 00:01},  Number = {12},  Own = {NLM},  Pages = {1647--1657},  Pl = {UNITED STATES},  Pmid = {9866200},  Pst = {ppublish},  Pt = {Journal Article; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print},  Rn = {0 (Plant Proteins); EC 4.1.1.39 (RbcL protein, plastid); EC 4.1.1.39 (Ribulose-Bisphosphate Carboxylase)},  Sb = {IM; S},  So = {Mol Biol Evol. 1998 Dec;15(12):1647-57.},  Stat = {MEDLINE},  Title = {Estimating the rate of evolution of the rate of molecular evolution.},  Volume = {15},  Year = {1998 Dec}}  @article{Kishino:2001ec,  Abstract = {Rates of molecular evolution vary over time and, hence, among lineages. In contrast, widely used methods for estimating divergence times from molecular sequence data assume constancy of rates. Therefore, methods for estimation of divergence times that incorporate rate variation are attractive. Improvements on a previously proposed Bayesian technique for divergence time estimation are described. New parameterization more effectively captures the phylogenetic structure of rate evolution on a tree. Fossil information and other evidence can now be included in Bayesian analyses in the form of constraints on divergence times. Simulation results demonstrate that the accuracy of divergence time estimation is substantially enhanced when constraints are included.},  Address = {Laboratory of Biometrics, Graduate School of Agriculture and Life Sciences, University of Tokyo, Tokyo, Japan. [email protected]},  Au = {Kishino, H and Thorne, JL and Bruno, WJ},  Author = {Kishino, H and Thorne, J L and Bruno, W J},  Da = {20010314},  Date-Added = {2008-11-28 18:43:16 -0800},  Date-Modified = {2008-11-28 18:43:16 -0800},  Dcom = {20010614},  Edat = {2001/03/07 10:00},  Gr = {GM45344/GM/United States NIGMS},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Lr = {20071114},  Mh = {Bayes Theorem; *Evolution; Fossils; *Models, Genetic; Probability},  Mhda = {2001/06/15 10:01},  Number = {3},  Own = {NLM},  Pages = {352--361},  Pl = {United States},  Pmid = {11230536},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Mol Biol Evol. 2001 Mar;18(3):352-61.},  Stat = {MEDLINE},  Title = {Performance of a divergence time estimation method under a probabilistic model of rate evolution.},  Volume = {18},  Year = {2001 Mar}}  @article{Thorne:2002ff,  Abstract = {Bayesian methods for estimating evolutionary divergence times are extended to multigene data sets, and a technique is described for detecting correlated changes in evolutionary rates among genes. Simulations are employed to explore the effect of multigene data on divergence time estimation, and the methodology is illustrated with a previously published data set representing diverse plant taxa. The fact that evolutionary rates and times are confounded when sequence data are compared is emphasized and the importance of fossil information for disentangling rates and times is stressed.},  Au = {Thorne, JL and Kishino, H},  Author = {Thorne, Jeffrey L and Kishino, Hirohisa},  Da = {20021024},  Date-Added = {2008-11-28 18:43:05 -0800},  Date-Modified = {2014-07-06 00:40:45 +0000},  Dcom = {20030513},  Doi = {10.1080/10635150290102456},  Edat = {2002/10/25 04:00},  Issn = {1063-5157 (Print)},  Jid = {9302532},  Journal = {Syst Biol},  Jt = {Systematic biology},  Language = {eng},  Lr = {20061115},  Mh = {Algorithms; Bayes Theorem; *Evolution; Evolution, Molecular; Markov Chains; *Models, Genetic; Monte Carlo Method; *Phylogeny; Plants/genetics; Time Factors},  Mhda = {2003/05/14 05:00},  Number = {5},  Own = {NLM},  Pages = {689--702},  Pl = {England},  Pmid = {12396584},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Syst Biol. 2002 Oct;51(5):689-702.},  Stat = {MEDLINE},  Title = {Divergence time and evolutionary rate estimation with multilocus data.},  Volume = {51},  Year = {2002 Oct},  Bdsk-Url-1 = {http://dx.doi.org/10.1080/10635150290102456}}  @article{beerli1999,  Author = {Beerli, Peter and Felsenstein, J.},  Date-Modified = {2014-12-04 01:05:53 +0000},  Journal = {Genetics},  Number = {2},  Pages = {763},  Publisher = {Genetics Soc America},  Title = {{Maximum-likelihood estimation of migration rates and effective population numbers in two populations using a coalescent approach}},  Volume = {152},  Year = {1999}}  @article{Beerli:2001fe,  Abstract = {A maximum likelihood estimator based on the coalescent for unequal migration rates and different subpopulation sizes is developed. The method uses a Markov chain Monte Carlo approach to investigate possible genealogies with branch lengths and with migration events. Properties of the new method are shown by using simulated data from a four-population n-island model and a source-sink population model. Our estimation method as coded in migrate is tested against genetree; both programs deliver a very similar likelihood surface. The algorithm converges to the estimates fairly quickly, even when the Markov chain is started from unfavorable parameters. The method was used to estimate gene flow in the Nile valley by using mtDNA data from three human populations.},  Au = {Beerli, P and Felsenstein, J},  Author = {Beerli, Peter and Felsenstein, J.},  Da = {20010411},  Date-Added = {2008-11-28 18:40:20 -0800},  Date-Modified = {2014-12-04 01:05:47 +0000},  Dcom = {20010510},  Dep = {20010403},  Doi = {10.1073/pnas.081068098},  Edat = {2001/04/05 10:00},  Gr = {R01 GM 01989/GM/United States NIGMS; R01 GM 51929/GM/United States NIGMS},  Issn = {0027-8424 (Print)},  Jid = {7505876},  Journal = {Proc Natl Acad Sci U S A},  Jt = {Proceedings of the National Academy of Sciences of the United States of America},  Language = {eng},  Lr = {20071114},  Mh = {*Genetics, Population; Humans; Likelihood Functions; Markov Chains; Monte Carlo Method; *Population Density; *Transients and Migrants},  Mhda = {2001/05/22 10:01},  Number = {8},  Own = {NLM},  Pages = {4563--4568},  Phst = {2001/04/03 {$[$}aheadofprint{$]$}},  Pii = {081068098},  Pl = {United States},  Pmc = {PMC31874},  Pmid = {11287657},  Pst = {ppublish},  Pt = {Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4563-8. Epub 2001 Apr 3.},  Stat = {MEDLINE},  Title = {Maximum likelihood estimation of a migration matrix and effective population sizes in n subpopulations by using a coalescent approach.},  Volume = {98},  Year = {2001},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.081068098}}  @article{Beerli:2006pi,  Abstract = {Comparison of the performance and accuracy of different inference methods, such as maximum likelihood (ML) and Bayesian inference, is difficult because the inference methods are implemented in different programs, often written by different authors. Both methods were implemented in the program MIGRATE, that estimates population genetic parameters, such as population sizes and migration rates, using coalescence theory. Both inference methods use the same Markov chain Monte Carlo algorithm and differ from each other in only two aspects: parameter proposal distribution and maximization of the likelihood function. Using simulated datasets, the Bayesian method generally fares better than the ML approach in accuracy and coverage, although for some values the two approaches are equal in performance. MOTIVATION: The Markov chain Monte Carlo-based ML framework can fail on sparse data and can deliver non-conservative support intervals. A Bayesian framework with appropriate prior distribution is able to remedy some of these problems. RESULTS: The program MIGRATE was extended to allow not only for ML(-) maximum likelihood estimation of population genetics parameters but also for using a Bayesian framework. Comparisons between the Bayesian approach and the ML approach are facilitated because both modes estimate the same parameters under the same population model and assumptions.},  Au = {Beerli, P},  Author = {Beerli, Peter},  Da = {20060201},  Date-Added = {2008-11-28 18:40:12 -0800},  Date-Modified = {2014-07-06 00:40:01 +0000},  Dcom = {20060307},  Dep = {20051129},  Doi = {10.1093/bioinformatics/bti803},  Edat = {2005/12/01 09:00},  Issn = {1367-4803 (Print)},  Jid = {9808944},  Journal = {Bioinformatics},  Jt = {Bioinformatics (Oxford, England)},  Language = {eng},  Lr = {20061115},  Mh = {*Bayes Theorem; Chromosome Mapping/*methods; Computer Simulation; Evolution; Genetics, Population/*methods; *Likelihood Functions; *Models, Genetic; *Models, Statistical; Phylogeny; *Software},  Mhda = {2006/03/08 09:00},  Month = {Feb},  Number = {3},  Own = {NLM},  Pages = {341--345},  Phst = {2005/11/29 {$[$}aheadofprint{$]$}},  Pii = {bti803},  Pl = {England},  Pmid = {16317072},  Pst = {ppublish},  Pt = {Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Bioinformatics. 2006 Feb 1;22(3):341-5. Epub 2005 Nov 29.},  Stat = {MEDLINE},  Title = {Comparison of Bayesian and maximum-likelihood inference of population genetic parameters.},  Volume = {22},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/bti803}}  @article{Yang:2007xr,  Abstract = {PAML, currently in version 4, is a package of programs for phylogenetic analyses of DNA and protein sequences using maximum likelihood (ML). The programs may be used to compare and test phylogenetic trees, but their main strengths lie in the rich repertoire of evolutionary models implemented, which can be used to estimate parameters in models of sequence evolution and to test interesting biological hypotheses. Uses of the programs include estimation of synonymous and nonsynonymous rates (d(N) and d(S)) between two protein-coding DNA sequences, inference of positive Darwinian selection through phylogenetic comparison of protein-coding genes, reconstruction of ancestral genes and proteins for molecular restoration studies of extinct life forms, combined analysis of heterogeneous data sets from multiple gene loci, and estimation of species divergence times incorporating uncertainties in fossil calibrations. This note discusses some of the major applications of the package, which includes example data sets to demonstrate their use. The package is written in ANSI C, and runs under Windows, Mac OSX, and UNIX systems. It is available at -- (http://abacus.gene.ucl.ac.uk/software/paml.html).},  Address = {Department of Biology, Galton Laboratory, University College London, London, UK. [email protected]},  Au = {Yang, Z},  Author = {Yang, Ziheng},  Da = {20070803},  Date-Added = {2008-11-28 18:38:46 -0800},  Date-Modified = {2008-11-28 18:38:46 -0800},  Dcom = {20071029},  Dep = {20070504},  Doi = {10.1093/molbev/msm088},  Edat = {2007/05/08 09:00},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Mh = {Animals; Computer Simulation; *Likelihood Functions; Models, Genetic; *Phylogeny; Selection (Genetics); Software; Species Specificity; Variation (Genetics)},  Mhda = {2007/10/30 09:00},  Number = {8},  Own = {NLM},  Pages = {1586--1591},  Phst = {2007/05/04 {$[$}aheadofprint{$]$}},  Pii = {msm088},  Pl = {United States},  Pmid = {17483113},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Mol Biol Evol. 2007 Aug;24(8):1586-91. Epub 2007 May 4.},  Stat = {MEDLINE},  Title = {PAML 4: phylogenetic analysis by maximum likelihood.},  Volume = {24},  Year = {2007 Aug},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msm088}}  @article{Huelsenbeck:2001oz,  Abstract = {SUMMARY: The program MRBAYES performs Bayesian inference of phylogeny using a variant of Markov chain Monte Carlo. AVAILABILITY: MRBAYES, including the source code, documentation, sample data files, and an executable, is available at http://brahms.biology.rochester.edu/software.html.},  Address = {Department of Biology, University of Rochester, Rochester, NY 14627, USA. [email protected]},  Au = {Huelsenbeck, JP and Ronquist, F},  Author = {Huelsenbeck, J P and Ronquist, F},  Da = {20010828},  Date-Added = {2008-11-28 18:37:14 -0800},  Date-Modified = {2008-11-28 18:37:14 -0800},  Dcom = {20011204},  Edat = {2001/08/29 10:00},  Issn = {1367-4803 (Print)},  Jid = {9808944},  Journal = {Bioinformatics},  Jt = {Bioinformatics (Oxford, England)},  Language = {eng},  Lr = {20061115},  Mh = {Algorithms; *Bayes Theorem; Computational Biology; Markov Chains; *Phylogeny; *Software},  Mhda = {2002/01/05 10:01},  Number = {8},  Own = {NLM},  Pages = {754--755},  Pl = {England},  Pmid = {11524383},  Pst = {ppublish},  Pt = {Journal Article; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Bioinformatics. 2001 Aug;17(8):754-5.},  Stat = {MEDLINE},  Title = {{MrBayes}: Bayesian inference of phylogenetic trees.},  Volume = {17},  Year = {2001 Aug}}  @article{Ronquist2003,  Au = {Ronquist, F and Huelsenbeck, JP},  Author = {Ronquist, Fredrik and Huelsenbeck, John P},  Da = {20030812},  Date-Added = {2008-11-28 18:37:11 -0800},  Date-Modified = {2014-07-05 08:50:12 +0000},  Dcom = {20040428},  Edat = {2003/08/13 05:00},  Issn = {1367-4803 (Print)},  Jid = {9808944},  Journal = {Bioinformatics},  Jt = {Bioinformatics (Oxford, England)},  Language = {eng},  Lr = {20061115},  Mh = {*Algorithms; Bayes Theorem; *Evolution, Molecular; Gene Expression Profiling/*methods; *Models, Genetic; *Models, Statistical; *Phylogeny; Sequence Alignment/*methods; Sequence Homology; Software; Stochastic Processes},  Mhda = {2004/04/29 05:00},  Month = {8},  Number = {12},  Own = {NLM},  Pages = {1572--1574},  Pl = {England},  Pmid = {12912839},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Bioinformatics. 2003 Aug 12;19(12):1572-4.},  Stat = {MEDLINE},  Title = {{MrBayes 3}: Bayesian phylogenetic inference under mixed models.},  Volume = {19},  Year = {2003}}  @article{Drummond:2001yf,  Abstract = {It is frequently true that molecular sequences do not evolve in a strictly clocklike manner. Instead, substitution rate may vary for a number of reasons, including changes in selection pressure and effective population size, as well as changes in mean generation time. Here we present two new methods for estimating stepwise changes in substitution rates when serially sampled molecular sequences are available. These methods are based on multiple rates with dated tips (MRDT) models and allow different rates to be estimated for different intervals of time. These intervals may correspond to the sampling intervals or to a priori--defined intervals that are not coincident with the times the serial samples are obtained. Two methods for obtaining estimates of multiple rates are described. The first is an extension of the phylogeny-based maximum-likelihood estimation procedure introduced by Rambaut. The second is a new parameterization of the pairwise distance least-squares procedure used by Drummond and Rodrigo. The utility of these methods is demonstrated on a genealogy of HIV sequences obtained at five different sampling times from a single patient over a period of 34 months.},  Au = {Drummond, A and Forsberg, R and Rodrigo, AG},  Author = {Drummond, A. J. and Forsberg, R. and Rodrigo, A. G.},  Da = {20010622},  Date-Added = {2008-11-28 10:43:42 -0800},  Date-Modified = {2014-07-06 00:56:50 +0000},  Dcom = {20010927},  Edat = {2001/06/23 10:00},  Gr = {GM59174/GM/United States NIGMS},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Lr = {20071114},  Mh = {Anti-HIV Agents/therapeutic use; *Evolution, Molecular; Genes, env; *Genetic Techniques; HIV Infections/drug therapy/virology; HIV-1/drug effects/genetics/isolation \& purification; Humans; Least-Squares Analysis; Likelihood Functions; *Models, Genetic; Time Factors; Zidovudine/therapeutic use},  Mhda = {2001/09/28 10:01},  Number = {7},  Own = {NLM},  Pages = {1365--1371},  Pl = {United States},  Pmid = {11420374},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print},  Rn = {0 (Anti-HIV Agents); 30516-87-1 (Zidovudine)},  Sb = {IM},  So = {Mol Biol Evol. 2001 Jul;18(7):1365-71.},  Stat = {MEDLINE},  Title = {The inference of stepwise changes in substitution rates using serial sequence samples.},  Volume = {18},  Year = {2001}}  @article{Drummond:2001sf,  Abstract = {Phylogenetic Analysis Library (PAL) is a collection of Java classes for use in molecular evolution and phylogenetics. PAL provides a modular environment for the rapid construction of both special-purpose and general analysis programs. PAL version 1.1 consists of 145 public classes or interfaces in 13 packages, including classes for models of character evolution, maximum-likelihood estimation, and the coalescent, with a total of more than 27000 lines of code. The PAL project is set up as a collaborative project to facilitate contributions from other researchers. AVAILIABILTY: The program is free and is available at http://www.pal-project.org. It requires Java 1.1 or later. PAL is licensed under the GNU General Public License.},  Address = {School of Biological Sciences, University of Auckland, 3A Symonds Street, Auckland, New Zealand. [email protected]},  Au = {Drummond, A and Strimmer, K},  Author = {Drummond, A. J. and Strimmer, K},  Da = {20010712},  Date-Added = {2008-11-28 10:43:39 -0800},  Date-Modified = {2014-07-06 00:49:52 +0000},  Dcom = {20011204},  Edat = {2001/07/13 10:00},  Gr = {GM59174/GM/United States NIGMS},  Issn = {1367-4803 (Print)},  Jid = {9808944},  Journal = {Bioinformatics},  Jt = {Bioinformatics (Oxford, England)},  Language = {eng},  Lr = {20071114},  Mh = {Computational Biology; *Evolution, Molecular; Likelihood Functions; *Phylogeny; *Software},  Mhda = {2002/01/05 10:01},  Number = {7},  Own = {NLM},  Pages = {662--663},  Pl = {England},  Pmid = {11448888},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print},  Sb = {IM},  So = {Bioinformatics. 2001 Jul;17(7):662-3.},  Stat = {MEDLINE},  Title = {PAL: an object-oriented programming library for molecular evolution and phylogenetics.},  Volume = {17},  Year = {2001}}  @article{Biek:2003hb,  Abstract = {Within the large body of research on retroviruses, the distribution and evolution of endemic retroviruses in natural host populations have so far received little attention. In this study, the epidemiology, genetic diversity, and molecular evolution of feline immunodeficiency virus specific to cougars (FIVpco) was examined using blood samples collected over several years from a free-ranging cougar population in the western United States. The virus prevalence was 58% in this population (n = 52) and increased significantly with host age. Based on phylogenetic analysis of fragments of envelope (env) and polymerase (pol) genes, two genetically distinct lineages of FIVpco were found to cooccur in the population but not in the same individuals. Within each of the virus lineages, geographically nearby isolates formed monophyletic clusters of closely related viruses. Sequence diversity for env within a host rarely exceeded 1%, and the evolution of this gene was dominated by purifying selection. For both pol and env, our data indicate mean rates of molecular evolution of 1 to 3% per 10 years. These results support the premise that FIVpco is well adapted to its cougar host and provide a basis for comparing lentivirus evolution in endemic and epidemic infections in natural hosts.},  Address = {Wildlife Biology Program, University of Montana, Missoula, Montana 59812, USA.},  Au = {Biek, R and Rodrigo, AG and Holley, D and Drummond, A and Anderson CR, Jr and Ross, HA and Poss, M},  Author = {Biek, Roman and Rodrigo, Allen G and Holley, David and Drummond, Alexei J. and Anderson, Charles R Jr and Ross, Howard A and Poss, Mary},  Da = {20030813},  Date-Added = {2008-11-28 10:43:18 -0800},  Date-Modified = {2014-07-06 00:52:12 +0000},  Dcom = {20030924},  Edat = {2003/08/14 05:00},  Issn = {0022-538X (Print)},  Jid = {0113724},  Journal = {J Virol},  Jt = {Journal of virology},  Language = {eng},  Lr = {20061115},  Mh = {Animals; Antibodies, Viral/blood; Base Sequence; Carnivora/*virology; DNA, Viral/genetics; Epidemiology, Molecular; Evolution, Molecular; Female; Genes, env; Genes, pol; Immunodeficiency Virus, Feline/*genetics/immunology/isolation \& purification; Lentivirus Infections/epidemiology/immunology/veterinary/virology; Male; Molecular Sequence Data; Phylogeny; United States/epidemiology; Variation (Genetics)},  Mhda = {2003/09/25 05:00},  Number = {17},  Own = {NLM},  Pages = {9578--9589},  Pl = {United States},  Pmc = {PMC187433},  Pmid = {12915571},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Rn = {0 (Antibodies, Viral); 0 (DNA, Viral)},  Sb = {IM},  So = {J Virol. 2003 Sep;77(17):9578-89.},  Stat = {MEDLINE},  Title = {Epidemiology, genetic diversity, and evolution of endemic feline immunodeficiency virus in a population of wild cougars.},  Volume = {77},  Year = {2003 Sep}}  @article{Rodrigo:2003jt,  Abstract = {The estimation of evolutionary rates from serially sampled sequences has recently been the focus of several studies. In this paper, we extend these analyzes to allow the estimation of a joint rate of substitution, omega, from several evolving populations from which serial samples are drawn. In the case of viruses evolving in different hosts, therapy may halt replication and therefore the accumulation of substitutions in the population. In such cases, it may be that only a proportion, p, of subjects are nonresponders who have viral populations that continue to evolve. We develop two likelihood-based procedures to jointly estimate p and omega, and empirical Bayes' tests of whether an individual should be classified as a responder or nonresponder. An example data set comprising HIV-1 partial envelope sequences from six patients on highly active antiretroviral therapy is analyzed.},  Address = {Computational and Evolutionary Biology Laboratory, School of Biological Sciences, University of Auckland, Auckland, New Zealand. [email protected]},  Au = {Rodrigo, AG and Goode, M and Forsberg, R and Ross, HA and Drummond, A},  Author = {Rodrigo, Allen G and Goode, Matthew and Forsberg, Roald and Ross, Howard A and Drummond, Alexei J.},  Da = {20031222},  Date-Added = {2008-11-28 10:43:09 -0800},  Date-Modified = {2014-07-06 00:50:37 +0000},  Dcom = {20041109},  Dep = {20030829},  Doi = {10.1093/molbev/msg215},  Edat = {2003/09/02 05:00},  Gr = {R01 GM59174/GM/United States NIGMS; R01-GM60729/GM/United States NIGMS},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Lr = {20071114},  Mh = {Algorithms; Antiretroviral Therapy, Highly Active/statistics \& numerical data; Bayes Theorem; *Evolution, Molecular; HIV-1/genetics; Humans; Likelihood Functions; Models, Genetic; Phylogeny},  Mhda = {2004/11/13 09:00},  Number = {12},  Own = {NLM},  Pages = {2010--2018},  Phst = {2003/08/29 {$[$}aheadofprint{$]$}},  Pii = {msg215},  Pl = {United States},  Pmid = {12949147},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Mol Biol Evol. 2003 Dec;20(12):2010-8. Epub 2003 Aug 29.},  Stat = {MEDLINE},  Title = {Inferring evolutionary rates using serially sampled sequences from several populations.},  Volume = {20},  Year = {2003 Dec},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msg215}}  @article{Bunce:2003pi,  Abstract = {The ratite moa (Aves; Dinornithiformes) were massive graviportal browsers weighing up to 250 kg (ref. 1) that dominated the New Zealand biota until their extinction approximately 500 yr ago. Despite an extensive Quaternary fossil record, moa taxonomy remains problematic and currently 11 species are recognized. Three Dinornis species were found throughout New Zealand and differed markedly in size (1-2 m height at back) and mass (from approximately 34 to 242 kg). Surprisingly, ancient mitochondrial DNA sequences show that the three species were genetically indistinguishable within each island, but formed separate North and South Island clades. Here we show, using the first sex-linked nuclear sequences from an extinct species, that on each island the three morphological forms actually represent just one species, whose size varied markedly according to sex and habitat. The largest females in this example of extreme reversed sexual size dimorphism were about 280% the weight and 150% the height of the largest males, which is unprecedented among birds and terrestrial mammals. The combination of molecular and palaeontological data highlights the difficulties of analysing extinct groups, even those with detailed fossil records.},  Au = {Bunce, M and Worthy, TH and Ford, T and Hoppitt, W and Willerslev, E and Drummond, A and Cooper, A},  Author = {Bunce, Michael and Worthy, Trevor H and Ford, Tom and Hoppitt, Will and Willerslev, Eske and Drummond, Alexei J. and Cooper, Alan},  Da = {20030911},  Date-Added = {2008-11-28 10:43:07 -0800},  Date-Modified = {2014-07-06 00:51:29 +0000},  Dcom = {20030924},  Doi = {10.1038/nature01871},  Edat = {2003/09/12 05:00},  Issn = {1476-4687 (Electronic)},  Jid = {0410462},  Journal = {Nature},  Jt = {Nature},  Language = {eng},  Lr = {20061115},  Mh = {Animals; *Body Constitution; Body Weight; Bone and Bones/anatomy \& histology; DNA, Mitochondrial/genetics; *Ecosystem; Evolution; Female; *Fossils; Geography; Male; Molecular Sequence Data; New Zealand; Palaeognathae/*anatomy \& histology/classification/genetics; Phylogeny; *Sex Characteristics; Sex Determination (Analysis); Time Factors},  Mhda = {2003/09/25 05:00},  Number = {6954},  Own = {NLM},  Pages = {172--175},  Phst = {2003/03/06 {$[$}received{$]$}; 2003/06/23 {$[$}accepted{$]$}},  Pii = {nature01871},  Pl = {England},  Pmid = {12968178},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Rn = {0 (DNA, Mitochondrial)},  Sb = {IM},  Si = {GENBANK/AY326127; GENBANK/AY326128; GENBANK/AY326129; GENBANK/AY326130; GENBANK/AY326131; GENBANK/AY326132; GENBANK/AY326133; GENBANK/AY326134; GENBANK/AY326135; GENBANK/AY326136; GENBANK/AY326137; GENBANK/AY326138; GENBANK/AY326139; GENBANK/AY326140; GENBANK/AY326141; GENBANK/AY326142; GENBANK/AY326143; GENBANK/AY326144; GENBANK/AY326145; GENBANK/AY326146; GENBANK/AY326147; GENBANK/AY326148; GENBANK/AY326149; GENBANK/AY326150; GENBANK/AY326151; GENBANK/AY326152; GENBANK/AY326153; GENBANK/AY326154; GENBANK/AY326155; GENBANK/AY326156; GENBANK/AY326157; GENBANK/AY326158; GENBANK/AY326159; GENBANK/AY326160; GENBANK/AY326161; GENBANK/AY326162; GENBANK/AY326163; GENBANK/AY326164; GENBANK/AY326165; GENBANK/AY326166; GENBANK/AY326167; GENBANK/AY326168; GENBANK/AY326169; GENBANK/AY326170; GENBANK/AY326171; GENBANK/AY326172; GENBANK/AY326173; GENBANK/AY326174; GENBANK/AY326175; GENBANK/AY326176; GENBANK/AY326177; GENBANK/AY326178; GENBANK/AY326179; GENBANK/AY326180; GENBANK/AY326181; GENBANK/AY326182; GENBANK/AY326183; GENBANK/AY326184; GENBANK/AY326185; GENBANK/AY326186; GENBANK/AY326187; GENBANK/AY326188; GENBANK/AY326189; GENBANK/AY326190; GENBANK/AY326191; GENBANK/AY326192; GENBANK/AY326193},  So = {Nature. 2003 Sep 11;425(6954):172-5.},  Stat = {MEDLINE},  Title = {Extreme reversed sexual size dimorphism in the extinct New Zealand moa Dinornis.},  Volume = {425},  Year = {2003},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature01871}}  @article{Drummond2003inference,  Abstract = {The processes of mutation and nucleotide substitution contribute to the observed variability in virulence, transmission and persistence of viral pathogens. Since most viruses evolve many times faster than their human hosts, we are in the unusual position of being able to measure these processes directly by comparing viral genes that have been isolated and sequenced at different points in time. The analysis of such data requires the use of specific statistical methods that take into account the shared ancestry of the sequences and the randomness inherent in the process of nucleotide substitution. In this paper we describe the various statistical methods for estimating evolutionary rates, which can be classified into three general approaches: linear regression, maximum likelihood, and Bayesian inference. We discuss the advantages and shortcomings of each approach and illustrate their use through the analysis of two example viruses; human immunodeficiency virus type 1 and dengue virus serotype 4. Reliable estimates of viral substitution rates have many important applications in population genetics and phylogenetics, including dating evolutionary events and divergence times, estimating demographic parameters such as population size and generation time, and investigating the effect of natural selection on molecular evolution.},  Au = {Drummond, A. and Pybus, O. G. and Rambaut, A.},  Author = {Drummond, Alexei J. and Pybus, Oliver G and Rambaut, Andrew},  Da = {20040108},  Date-Added = {2008-11-28 10:43:05 -0800},  Date-Modified = {2014-08-02 22:08:22 +0000},  Dcom = {20040122},  Edat = {2004/01/09 05:00},  Issn = {0065-308X (Print)},  Jid = {0370435},  Journal = {Adv Parasitol},  Jt = {Advances in parasitology},  Lr = {20061115},  Mh = {Base Sequence; *Evolution, Molecular; *Genes, Viral; Humans; Models, Statistical; Viruses/*genetics},  Mhda = {2004/01/24 05:00},  Own = {NLM},  Pages = {331--358},  Pl = {England},  Pmid = {14711090},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Review},  Pubm = {Print},  Rf = {62},  Sb = {IM},  So = {Adv Parasitol. 2003;54:331-58.},  Stat = {MEDLINE},  Title = {Inference of viral evolutionary rates from molecular sequences.},  Volume = {54},  Year = {2003}}  @article{Hon:2006ph,  Abstract = {Infectious bursal disease virus (IBDV) is a birnavirus causing immunosuppressive disease in chickens. Emergence of the very virulent form of IBDV (vvIBDV) in the late 1980s dramatically changed the epidemiology of the disease. In this study, we investigated the phylogenetic origins of its genome segments and estimated the time of emergence of their most recent common ancestors. Moreover, with recently developed coalescence techniques, we reconstructed the past population dynamics of vvIBDV and timed the onset of its expansion to the late 1980s. Our analysis suggests that genome segment A of vvIBDV emerged at least 20 years before its expansion, which argues against the hypothesis that mutation of genome segment A is the major contributing factor in the emergence and expansion of vvIBDV. Alternatively, the phylogeny of genome segment B suggests a possible reassortment event estimated to have taken place around the mid-1980s, which seems to coincide with its expansion within approximately 5 years. We therefore hypothesize that the reassortment of genome segment B initiated vvIBDV expansion in the late 1980s, possibly by enhancing the virulence of the virus synergistically with its existing genome segment A. This report reveals the possible mechanisms leading to the emergence and expansion of vvIBDV, which would certainly provide insights into the scope of surveillance and prevention efforts regarding the disease.},  Address = {Department of Zoology, The University of Hong Kong, China.},  Au = {Hon, CC and Lam, TY and Drummond, A and Rambaut, A and Lee, YF and Yip, CW and Zeng, F and Lam, PY and Ng, PT and Leung, FC},  Author = {Hon, Chung-Chau and Lam, Tsan-Yuk and Drummond, Alexei J. and Rambaut, Andrew and Lee, Yiu-Fai and Yip, Chi-Wai and Zeng, Fanya and Lam, Pui-Yi and Ng, Patrick T W and Leung, Frederick C C},  Da = {20060816},  Date-Added = {2008-11-28 10:42:26 -0800},  Date-Modified = {2014-07-06 00:49:38 +0000},  Dcom = {20060925},  Doi = {10.1128/JVI.00585-06},  Edat = {2006/08/17 09:00},  Issn = {0022-538X (Print)},  Jid = {0113724},  Journal = {J Virol},  Jt = {Journal of virology},  Language = {eng},  Mh = {Animals; Birnaviridae Infections/epidemiology/*veterinary/virology; Chickens; Evolution, Molecular; *Genome, Viral; Infectious bursal disease virus/classification/*genetics/*pathogenicity; *Phylogeny; Poultry Diseases/epidemiology/virology; Reassortant Viruses/classification/*genetics/*pathogenicity; Time Factors; Virulence},  Mhda = {2006/09/26 09:00},  Number = {17},  Own = {NLM},  Pages = {8503--8509},  Pii = {80/17/8503},  Pl = {United States},  Pmc = {PMC1563883},  Pmid = {16912300},  Pst = {ppublish},  Pt = {Journal Article},  Pubm = {Print},  Sb = {IM},  So = {J Virol. 2006 Sep;80(17):8503-9.},  Stat = {MEDLINE},  Title = {Phylogenetic analysis reveals a correlation between the expansion of very virulent infectious bursal disease virus and reassortment of its genome segment B.},  Volume = {80},  Year = {2006 Sep},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.00585-06}}  @article{Lambert:2002gd,  Abstract = {Well-preserved subfossil bones of Adelie penguins, Pygoscelis adeliae, underlie existing and abandoned nesting colonies in Antarctica. These bones, dating back to more than 7000 years before the present, harbor some of the best-preserved ancient DNA yet discovered. From 96 radiocarbon-aged bones, we report large numbers of mitochondrial haplotypes, some of which appear to be extinct, given the 380 living birds sampled. We demonstrate DNA sequence evolution through time and estimate the rate of evolution of the hypervariable region I using a Markov chain Monte Carlo integration and a least-squares regression analysis. Our calculated rates of evolution are approximately two to seven times higher than previous indirect phylogenetic estimates.},  Au = {Lambert, DM and Ritchie, PA and Millar, CD and Holland, B and Drummond, AJ and Baroni, C},  Author = {Lambert, D M and Ritchie, P A and Millar, C D and Holland, B and Drummond, A J and Baroni, C},  Cin = {Science. 2002 Mar 22;295(5563):2197. PMID: 11910085},  Da = {20020322},  Date-Added = {2008-11-28 10:41:19 -0800},  Date-Modified = {2014-07-03 23:04:46 +0000},  Dcom = {20020404},  Doi = {10.1126/science.1068105},  Edat = {2002/03/23 10:00},  Issn = {1095-9203 (Electronic)},  Jid = {0404511},  Journal = {Science},  Jt = {Science (New York, N.Y.)},  Language = {eng},  Lr = {20070319},  Mh = {Animals; Antarctic Regions; Birds/*genetics; Bone and Bones/metabolism; Calibration; Carbon Radioisotopes; DNA, Mitochondrial/*genetics/isolation \& purification; Ecosystem; *Evolution, Molecular; Fossils; Haplotypes/genetics; Least-Squares Analysis; Markov Chains; Monte Carlo Method; Phylogeny; Polymerase Chain Reaction; Time Factors},  Mhda = {2002/04/18 10:01},  Number = {5563},  Own = {NLM},  Pages = {2270--2273},  Pii = {295/5563/2270},  Pl = {United States},  Pmid = {11910113},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print},  Rn = {0 (Carbon Radioisotopes); 0 (DNA, Mitochondrial)},  Sb = {IM},  So = {Science. 2002 Mar 22;295(5563):2270-3.},  Stat = {MEDLINE},  Title = {Rates of evolution in ancient DNA from Adelie penguins.},  Volume = {295},  Year = {2002},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1068105}}  @article{Pybus:2003la,  Abstract = {Hepatitis C virus (HCV) is a leading cause of liver cancer and cirrhosis, and Egypt has possibly the highest HCV prevalence worldwide. In this article we use a newly developed Bayesian inference framework to estimate the transmission dynamics of HCV in Egypt from sampled viral gene sequences, and to predict the public health impact of the virus. Our results indicate that the effective number of HCV infections in Egypt underwent rapid exponential growth between 1930 and 1955. The timing and speed of this spread provides quantitative genetic evidence that the Egyptian HCV epidemic was initiated and propagated by extensive antischistosomiasis injection campaigns. Although our results show that HCV transmission has since decreased, we conclude that HCV is likely to remain prevalent in Egypt for several decades. Our combined population genetic and epidemiological analysis provides detailed estimates of historical changes in Egyptian HCV prevalence. Because our results are consistent with a demographic scenario specified a priori, they also provide an objective test of inference methods based on the coalescent process.},  Au = {Pybus, OG and Drummond, AJ and Nakano, T and Robertson, BH and Rambaut, A},  Author = {Pybus, O G and Drummond, A J and Nakano, T and Robertson, B H and Rambaut, A},  Da = {20030319},  Date-Added = {2008-11-28 10:41:16 -0800},  Date-Modified = {2014-07-04 01:56:39 +0000},  Dcom = {20031023},  Edat = {2003/03/20 04:00},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Lr = {20061115},  Mh = {Bayes Theorem; Demography; Egypt/epidemiology; Hepacivirus/*genetics/pathogenicity; Hepatitis C/*epidemiology/*transmission; Humans; Iatrogenic Disease/epidemiology; Models, Genetic; Mutagenesis; Prevalence},  Mhda = {2003/10/24 05:00},  Month = {3},  Number = {3},  Own = {NLM},  Pages = {381--387},  Pl = {United States},  Pmid = {12644558},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Sb = {IM},  So = {Mol Biol Evol. 2003 Mar;20(3):381-7.},  Stat = {MEDLINE},  Title = {The epidemiology and iatrogenic transmission of hepatitis C virus in Egypt: a Bayesian coalescent approach.},  Volume = {20},  Year = {2003}}  @article{Strugnell:2004ek,  Au = {Strugnell, J and Norman, M and Drummond, AJ and Cooper, A},  Author = {Strugnell, Jan and Norman, Mark and Drummond, Alexei J and Cooper, Alan},  Da = {20040415},  Date-Added = {2008-11-28 10:41:13 -0800},  Date-Modified = {2008-11-28 10:41:13 -0800},  Dcom = {20040608},  Doi = {10.1016/j.cub.2004.03.048},  Edat = {2004/04/16 05:00},  Issn = {0960-9822 (Print)},  Jid = {9107782},  Journal = {Curr Biol},  Jt = {Current biology : CB},  Language = {eng},  Lr = {20061115},  Mh = {*Adaptation, Physiological; Animals; Base Sequence; Bayes Theorem; Environment; Likelihood Functions; Models, Genetic; Molecular Sequence Data; Octopodiformes/embryology/*genetics/physiology; *Phylogeny; Sequence Analysis, DNA; Time Factors},  Mhda = {2004/06/21 10:00},  Number = {8},  Own = {NLM},  Pages = {R300-1},  Pii = {S0960982204002258},  Pl = {England},  Pmid = {15084297},  Pst = {ppublish},  Pt = {Comparative Study; Letter},  Pubm = {Print},  Sb = {IM},  So = {Curr Biol. 2004 Apr 20;14(8):R300-1.},  Stat = {MEDLINE},  Title = {Neotenous origins for pelagic octopuses.},  Volume = {14},  Year = {2004 Apr 20},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cub.2004.03.048}}  @article{Cooper:2004qq,  Abstract = {Mitochondrial DNA sequences recovered from eight Neandertal specimens cannot be detected in either early fossil Europeans or in modern populations. This indicates that, if Neandertals made any genetic contribution at all to modern humans, it must have been limited, though the extent of the contribution cannot be resolved at present.},  Address = {Henry Wellcome Ancient Biomolecules Centre and Department of Zoology, University of Oxford, Oxford OX1 3PS, UK.},  Au = {Cooper, A and Drummond, AJ and Willerslev, E},  Author = {Cooper, Alan and Drummond, Alexei J and Willerslev, Eske},  Ci = {Copyright 2004 Elsevier Ltd.},  Da = {20040608},  Date-Added = {2008-11-28 10:41:09 -0800},  Date-Modified = {2008-11-28 10:41:09 -0800},  Dcom = {20040902},  Doi = {10.1016/j.cub.2004.05.037},  Edat = {2004/06/09 05:00},  Issn = {0960-9822 (Print)},  Jid = {9107782},  Journal = {Curr Biol},  Jt = {Current biology : CB},  Language = {eng},  Lr = {20051116},  Mh = {Animals; DNA, Mitochondrial/*genetics; *Fossils; Hominidae/*genetics; Humans; *Models, Genetic; Time Factors},  Mhda = {2004/09/03 05:00},  Number = {11},  Own = {NLM},  Pages = {R431-3},  Pii = {S0960982204003641},  Pl = {England},  Pmid = {15182692},  Pst = {ppublish},  Pt = {Journal Article; Review},  Pubm = {Print},  Rf = {17},  Rn = {0 (DNA, Mitochondrial)},  Sb = {IM},  So = {Curr Biol. 2004 Jun 8;14(11):R431-3.},  Stat = {MEDLINE},  Title = {Ancient DNA: would the real Neandertal please stand up?},  Volume = {14},  Year = {2004 Jun 8},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.cub.2004.05.037}}  @article{Lemey:2004uo,  Abstract = {HIV-1 group O originated through cross-species transmission of SIV from chimpanzees to humans and has established a relatively low prevalence in Central Africa. Here, we infer the population genetics and epidemic history of HIV-1 group O from viral gene sequence data and evaluate the effect of variable evolutionary rates and recombination on our estimates. First, model selection tools were used to specify suitable evolutionary and coalescent models for HIV group O. Second, divergence times and population genetic parameters were estimated in a Bayesian framework using Markov chain Monte Carlo sampling, under both strict and relaxed molecular clock methods. Our results date the origin of the group O radiation to around 1920 (1890-1940), a time frame similar to that estimated for HIV-1 group M. However, group O infections, which remain almost wholly restricted to Cameroon, show a slower rate of exponential growth during the twentieth century, explaining their lower current prevalence. To explore the effect of recombination, the Bayesian framework is extended to incorporate multiple unlinked loci. Although recombination can bias estimates of the time to the most recent common ancestor, this effect does not appear to be important for HIV-1 group O. In addition, we show that evolutionary rate estimates for different HIV genes accurately reflect differential selective constraints along the HIV genome.},  Address = {Rega Institute for Medical Research, KULeuven, B-3000 Leuven, Belgium. [email protected]},  Au = {Lemey, P and Pybus, OG and Rambaut, A and Drummond, AJ and Robertson, DL and Roques, P and Worobey, M and Vandamme, AM},  Author = {Lemey, Philippe and Pybus, Oliver G and Rambaut, Andrew and Drummond, Alexei J and Robertson, David L and Roques, Pierre and Worobey, Michael and Vandamme, Anne-Mieke},  Da = {20040728},  Date-Added = {2008-11-28 10:41:08 -0800},  Date-Modified = {2008-11-28 10:41:08 -0800},  Dcom = {20050224},  Doi = {10.1534/genetics.104.026666},  Edat = {2004/07/29 05:00},  Issn = {0016-6731 (Print)},  Jid = {0374636},  Journal = {Genetics},  Jt = {Genetics},  Language = {eng},  Lr = {20061115},  Mh = {Bayes Theorem; Cameroon; *Evolution, Molecular; *Genetics, Population; *Genome, Viral; HIV-1/*genetics; Humans; Likelihood Functions; *Models, Genetic; Phylogeny; Recombination, Genetic/genetics; Species Specificity; Viral Proteins/genetics},  Mhda = {2005/02/25 09:00},  Number = {3},  Own = {NLM},  Pages = {1059--1068},  Pii = {167/3/1059},  Pl = {United States},  Pmc = {PMC1470933},  Pmid = {15280223},  Pst = {ppublish},  Pt = {Comparative Study; Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Rn = {0 (Viral Proteins)},  Sb = {IM},  So = {Genetics. 2004 Jul;167(3):1059-68.},  Stat = {MEDLINE},  Title = {The molecular population genetics of HIV-1 group O.},  Volume = {167},  Year = {2004 Jul},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.104.026666}}  @article{leonard2002,  Author = {Leonard, J.A. and Wayne, R.K. and Wheeler, J. and Valadez, R. and Guillen, S. and Vila, C.},  Journal = {Science},  Number = {5598},  Pages = {1613},  Publisher = {AAAS},  Title = {{Ancient DNA evidence for Old World origin of New World dogs}},  Volume = {298},  Year = {2002}}  @article{Shapiro:2004xe,  Abstract = {The widespread extinctions of large mammals at the end of the Pleistocene epoch have often been attributed to the depredations of humans; here we present genetic evidence that questions this assumption. We used ancient DNA and Bayesian techniques to reconstruct a detailed genetic history of bison throughout the late Pleistocene and Holocene epochs. Our analyses depict a large diverse population living throughout Beringia until around 37,000 years before the present, when the population's genetic diversity began to decline dramatically. The timing of this decline correlates with environmental changes associated with the onset of the last glacial cycle, whereas archaeological evidence does not support the presence of large populations of humans in Eastern Beringia until more than 15,000 years later.},  Au = {Shapiro, B and Drummond, AJ and Rambaut, A and Wilson, MC and Matheus, PE and Sher, AV and Pybus, OG and Gilbert, MT and Barnes, I and Binladen, J and Willerslev, E and Hansen, AJ and Baryshnikov, GF and Burns, JA and Davydov, S and Driver, JC and Froese, DG and Harington, CR and Keddie, G and Kosintsev, P and Kunz, ML and Martin, LD and Stephenson, RO and Storer, J and Tedford, R and Zimov, S and Cooper, A},  Author = {Shapiro, Beth and Drummond, Alexei J and Rambaut, Andrew and Wilson, Michael C and Matheus, Paul E and Sher, Andrei V and Pybus, Oliver G and Gilbert, M Thomas P and Barnes, Ian and Binladen, Jonas and Willerslev, Eske and Hansen, Anders J and Baryshnikov, Gennady F and Burns, James A and Davydov, Sergei and Driver, Jonathan C and Froese, Duane G and Harington, C Richard and Keddie, Grant and Kosintsev, Pavel and Kunz, Michael L and Martin, Larry D and Stephenson, Robert O and Storer, John and Tedford, Richard and Zimov, Sergei and Cooper, Alan},  Cin = {Science. 2004 Nov 26;306(5701):1454. PMID: 15567821},  Da = {20041129},  Date-Added = {2008-11-28 10:41:06 -0800},  Date-Modified = {2014-07-06 00:40:24 +0000},  Dcom = {20041221},  Doi = {10.1126/science.1101074},  Edat = {2004/11/30 09:00},  Issn = {1095-9203 (Electronic)},  Jid = {0404511},  Journal = {Science},  Jt = {Science (New York, N.Y.)},  Language = {eng},  Lr = {20070319},  Mh = {Alaska; Animals; Bayes Theorem; *Bison/classification/genetics; Canada; China; *Climate; DNA, Mitochondrial/genetics; Environment; *Fossils; Genetics, Population; Human Activities; Humans; North America; Phylogeny; Population Dynamics; Sequence Analysis, DNA; Time; Variation (Genetics)},  Mhda = {2004/12/22 09:00},  Number = {5701},  Own = {NLM},  Pages = {1561--1565},  Pii = {306/5701/1561},  Pl = {United States},  Pmid = {15567864},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Rn = {0 (DNA, Mitochondrial)},  Sb = {IM},  So = {Science. 2004 Nov 26;306(5701):1561-5.},  Stat = {MEDLINE},  Title = {Rise and fall of the Beringian steppe bison.},  Volume = {306},  Year = {2004},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1101074}}  @article{Ho:2005rw,  Abstract = {In recent years, a number of phylogenetic methods have been developed for estimating molecular rates and divergence dates under models that relax the molecular clock constraint by allowing rate change throughout the tree. These methods are being used with increasing frequency, but there have been few studies into their accuracy. We tested the accuracy of several relaxed-clock methods (penalized likelihood and Bayesian inference using various models of rate change) using nucleotide sequences simulated on a nine-taxon tree. When the sequences evolved with a constant rate, the methods were able to infer rates accurately, but estimates were more precise when a molecular clock was assumed. When the sequences evolved under a model of auto-correlated rate change, rates were accurately estimated using penalized likelihood and by Bayesian inference using lognormal and exponential models of rate change, while other models did not perform as well. When the sequences evolved under a model of uncorrelated rate change, only Bayesian inference using an exponential rate model performed well. Collectively, the results provide a strong recommendation for using the exponential model of rate change if a conservative approach to divergence time estimation is required. A case study is presented in which we use a simulation-based approach to examine the hypothesis of elevated rates in the Cambrian period, and it is found that these high rate estimates might be an artifact of the rate estimation method. If this bias is present, then the ages of metazoan divergences would be systematically underestimated. The results of this study have implications for studies of molecular rates and divergence dates.},  Address = {Henry Wellcome Ancient Biomolecules Centre, Oxford, United Kingdom. [email protected]},  Au = {Ho, SY and Phillips, MJ and Drummond, AJ and Cooper, A},  Author = {Ho, Simon Y W and Phillips, Matthew J and Drummond, Alexei J and Cooper, Alan},  Da = {20050413},  Date-Added = {2008-11-28 10:41:04 -0800},  Date-Modified = {2008-11-28 10:41:04 -0800},  Dcom = {20050830},  Dep = {20050309},  Doi = {10.1093/molbev/msi125},  Edat = {2005/03/11 09:00},  Gr = {United Kingdom Wellcome Trust},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Lr = {20070813},  Mh = {*Algorithms; Animals; Bayes Theorem; *Evolution, Molecular; Invertebrates/*genetics/*radiation effects; Likelihood Functions; Markov Chains; *Models, Genetic; Phylogeny; Time Factors},  Mhda = {2005/09/01 09:00},  Number = {5},  Own = {NLM},  Pages = {1355--1363},  Phst = {2005/03/09 {$[$}aheadofprint{$]$}},  Pii = {msi125},  Pl = {United States},  Pmid = {15758207},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Mol Biol Evol. 2005 May;22(5):1355-63. Epub 2005 Mar 9.},  Stat = {MEDLINE},  Title = {Accuracy of rate estimation using relaxed-clock models with a critical focus on the early metazoan radiation.},  Volume = {22},  Year = {2005 May},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msi125}}  @article{Ho:2005rc,  Abstract = {Studies of molecular evolutionary rates have yielded a wide range of rate estimates for various genes and taxa. Recent studies based on population-level and pedigree data have produced remarkably high estimates of mutation rate, which strongly contrast with substitution rates inferred in phylogenetic (species-level) studies. Using Bayesian analysis with a relaxed-clock model, we estimated rates for three groups of mitochondrial data: avian protein-coding genes, primate protein-coding genes, and primate d-loop sequences. In all three cases, we found a measurable transition between the high, short-term (< 1-2 Myr) mutation rate and the low, long-term substitution rate. The relationship between the age of the calibration and the rate of change can be described by a vertically translated exponential decay curve, which may be used for correcting molecular date estimates. The phylogenetic substitution rates in mitochondria are approximately 0.5% per million years for avian protein-coding sequences and 1.5% per million years for primate protein-coding and d-loop sequences. Further analyses showed that purifying selection offers the most convincing explanation for the observed relationship between the estimated rate and the depth of the calibration. We rule out the possibility that it is a spurious result arising from sequence errors, and find it unlikely that the apparent decline in rates over time is caused by mutational saturation. Using a rate curve estimated from the d-loop data, several dates for last common ancestors were calculated: modern humans and Neandertals (354 ka; 222-705 ka), Neandertals (108 ka; 70-156 ka), and modern humans (76 ka; 47-110 ka). If the rate curve for a particular taxonomic group can be accurately estimated, it can be a useful tool for correcting divergence date estimates by taking the rate decay into account. Our results show that it is invalid to extrapolate molecular rates of change across different evolutionary timescales, which has important consequences for studies of populations, domestication, conservation genetics, and human evolution.},  Address = {Henry Wellcome Ancient Biomolecules Centre, Department of Zoology, University of Oxford, Oxford, United Kingdom. [email protected]},  Au = {Ho, SY and Phillips, MJ and Cooper, A and Drummond, AJ},  Author = {Ho, Simon Y W and Phillips, Matthew J and Cooper, Alan and Drummond, Alexei J},  Da = {20050606},  Date-Added = {2008-11-28 10:41:03 -0800},  Date-Modified = {2008-11-28 10:41:03 -0800},  Dcom = {20051214},  Dep = {20050406},  Doi = {10.1093/molbev/msi145},  Edat = {2005/04/09 09:00},  Gr = {United Kingdom Wellcome Trust},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Lr = {20070813},  Mh = {Animals; Bayes Theorem; Birds/genetics; DNA, Mitochondrial/*genetics; *Evolution, Molecular; *Genetics, Population; Hominidae/genetics; Humans/genetics; Mutation; *Phylogeny; Primates/genetics; Species Specificity; Time Factors; Variation (Genetics)},  Mhda = {2005/12/15 09:00},  Number = {7},  Own = {NLM},  Pages = {1561--1568},  Phst = {2005/04/06 {$[$}aheadofprint{$]$}},  Pii = {msi145},  Pl = {United States},  Pmid = {15814826},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Rn = {0 (DNA, Mitochondrial)},  Sb = {IM},  So = {Mol Biol Evol. 2005 Jul;22(7):1561-8. Epub 2005 Apr 6.},  Stat = {MEDLINE},  Title = {Time dependency of molecular rate estimates and systematic overestimation of recent divergence times.},  Volume = {22},  Year = {2005 Jul},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msi145}}  @article{Strugnell:2005qr,  Address = {Molecular Evolution, Department of Zoology, South Parks Road, Oxford OX1 3PS, UK. [email protected]},  Au = {Strugnell, J and Norman, M and Jackson, J and Drummond, AJ and Cooper, A},  Author = {Strugnell, Jan and Norman, Mark and Jackson, Jennifer and Drummond, Alexei J and Cooper, Alan},  Da = {20051014},  Date-Added = {2008-11-28 10:41:02 -0800},  Date-Modified = {2008-11-28 10:41:02 -0800},  Dcom = {20051223},  Dep = {20050602},  Doi = {10.1016/j.ympev.2005.03.020},  Edat = {2005/06/07 09:00},  Issn = {1055-7903 (Print)},  Jid = {9304400},  Journal = {Mol Phylogenet Evol},  Jt = {Molecular phylogenetics and evolution},  Language = {eng},  Lr = {20061115},  Mh = {Animals; Bayes Theorem; Cephalopoda/*classification/*genetics; *Evolution, Molecular; *Genes; *Phylogeny},  Mhda = {2005/12/24 09:00},  Number = {2},  Own = {NLM},  Pages = {426--441},  Phst = {2004/12/09 {$[$}received{$]$}; 2005/03/03 {$[$}revised{$]$}; 2005/03/15 {$[$}accepted{$]$}; 2005/06/02 {$[$}aheadofprint{$]$}},  Pii = {S1055-7903(05)00094-1},  Pl = {United States},  Pmid = {15935706},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Mol Phylogenet Evol. 2005 Nov;37(2):426-41. Epub 2005 Jun 2.},  Stat = {MEDLINE},  Title = {Molecular phylogeny of coleoid cephalopods (Mollusca: Cephalopoda) using a multigene approach; the effect of data partitioning on resolving phylogenies in a Bayesian framework.},  Volume = {37},  Year = {2005 Nov},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.ympev.2005.03.020}}  @article{Forsberg:2005qd,  Address = {Bioinformatics Research Center, Department of Genetics and Ecology, University of Aarhus, Arhus, Denmark. [email protected]},  Au = {Forsberg, R and Drummond, AJ and Hein, J},  Author = {Forsberg, Roald and Drummond, Alexei J and Hein, Jotun},  Da = {20050815},  Date-Added = {2008-11-28 10:40:57 -0800},  Date-Modified = {2008-11-28 10:40:57 -0800},  Dcom = {20060612},  Dep = {20050616},  Doi = {10.1186/1471-2156-6-35},  Edat = {2005/06/18 09:00},  Gr = {1-R01-GM60729-01/GM/United States NIGMS},  Issn = {1471-2156 (Electronic)},  Jid = {100966978},  Journal = {BMC Genet},  Jt = {BMC genetics},  Language = {eng},  Lr = {20071114},  Mh = {Animals; DNA, Mitochondrial/genetics; *Evolution; Humans; *Models, Genetic; *Mutation; Pedigree; Probability; Time},  Mhda = {2006/06/13 09:00},  Own = {NLM},  Pages = {35},  Phst = {2004/10/19 {$[$}received{$]$}; 2005/06/16 {$[$}accepted{$]$}; 2005/06/16 {$[$}aheadofprint{$]$}},  Pii = {1471-2156-6-35},  Pl = {England},  Pmc = {PMC1185533},  Pmid = {15960847},  Pst = {epublish},  Pt = {Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Electronic},  Rn = {0 (DNA, Mitochondrial)},  Sb = {IM},  So = {BMC Genet. 2005 Jun 16;6:35.},  Stat = {MEDLINE},  Title = {Tree measures and the number of segregating sites in time-structured population samples.},  Volume = {6},  Year = {2005},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2156-6-35}}  @article{Shapiro:2006hl,  Abstract = {Although phylogenetic inference of protein-coding sequences continues to dominate the literature, few analyses incorporate evolutionary models that consider the genetic code. This problem is exacerbated by the exclusion of codon-based models from commonly employed model selection techniques, presumably due to the computational cost associated with codon models. We investigated an efficient alternative to standard nucleotide substitution models, in which codon position (CP) is incorporated into the model. We determined the most appropriate model for alignments of 177 RNA virus genes and 106 yeast genes, using 11 substitution models including one codon model and four CP models. The majority of analyzed gene alignments are best described by CP substitution models, rather than by standard nucleotide models, and without the computational cost of full codon models. These results have significant implications for phylogenetic inference of coding sequences as they make it clear that substitution models incorporating CPs not only are a computationally realistic alternative to standard models but may also frequently be statistically superior.},  Au = {Shapiro, B and Rambaut, A and Drummond, AJ},  Author = {Shapiro, Beth and Rambaut, Andrew and Drummond, Alexei J},  Da = {20051205},  Date-Added = {2008-11-28 10:40:55 -0800},  Date-Modified = {2008-11-28 10:40:55 -0800},  Dcom = {20060810},  Dep = {20050921},  Doi = {10.1093/molbev/msj021},  Edat = {2005/09/24 09:00},  Gr = {United Kingdom Wellcome Trust},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Lr = {20070813},  Mh = {Classification/*methods; Codon/genetics; *Models, Genetic; *Phylogeny; Proteins/*genetics; RNA Viruses/genetics; Sequence Alignment/methods; Yeasts/genetics},  Mhda = {2006/08/11 09:00},  Number = {1},  Own = {NLM},  Pages = {7--9},  Phst = {2005/09/21 {$[$}aheadofprint{$]$}},  Pii = {msj021},  Pl = {United States},  Pmid = {16177232},  Pst = {ppublish},  Pt = {Comparative Study; Letter; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Rn = {0 (Codon); 0 (Proteins)},  Sb = {IM},  So = {Mol Biol Evol. 2006 Jan;23(1):7-9. Epub 2005 Sep 21.},  Stat = {MEDLINE},  Title = {Choosing appropriate substitution models for the phylogenetic analysis of protein-coding sequences.},  Volume = {23},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msj021}}  @article{Biek:2006db,  Address = {Wildlife Biology Program, University of Montana, Missoula, MT 59812, USA. [email protected]},  Au = {Biek, R and Drummond, AJ and Poss, M},  Author = {Biek, Roman and Drummond, Alexei J and Poss, Mary},  Da = {20060127},  Date-Added = {2008-11-28 10:40:54 -0800},  Date-Modified = {2008-11-28 10:40:54 -0800},  Dcom = {20060203},  Doi = {10.1126/science.1121360},  Edat = {2006/01/28 09:00},  Issn = {1095-9203 (Electronic)},  Jid = {0404511},  Journal = {Science},  Jt = {Science (New York, N.Y.)},  Language = {eng},  Lr = {20070319},  Mh = {Alberta/epidemiology; Animals; Bayes Theorem; British Columbia/epidemiology; Ecosystem; *Evolution, Molecular; Genes, env; Genes, pol; Geography; Immunodeficiency Virus, Feline/*classification/*genetics; Lentivirus Infections/epidemiology/*veterinary/virology; Microsatellite Repeats; Molecular Sequence Data; Montana/epidemiology; Phylogeny; Population Dynamics; *Puma/genetics/virology; Time Factors; Wyoming/epidemiology},  Mhda = {2006/02/04 09:00},  Number = {5760},  Own = {NLM},  Pages = {538--541},  Pii = {311/5760/538},  Pl = {United States},  Pmid = {16439664},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.},  Pubm = {Print},  Sb = {IM},  Si = {GENBANK/DQ106985; GENBANK/DQ106986; GENBANK/DQ106987; GENBANK/DQ106988; GENBANK/DQ106989; GENBANK/DQ106990; GENBANK/DQ106991; GENBANK/DQ106992; GENBANK/DQ106993; GENBANK/DQ106994; GENBANK/DQ106995; GENBANK/DQ106996; GENBANK/DQ106997; GENBANK/DQ106998; GENBANK/DQ106999; GENBANK/DQ107000; GENBANK/DQ107001; GENBANK/DQ107002; GENBANK/DQ107003; GENBANK/DQ107004; GENBANK/DQ107005; GENBANK/DQ107006; GENBANK/DQ107007; GENBANK/DQ107008; GENBANK/DQ107009; GENBANK/DQ107010; GENBANK/DQ107011; GENBANK/DQ107012; GENBANK/DQ107013; GENBANK/DQ107014; GENBANK/DQ107015; GENBANK/DQ107016; GENBANK/DQ107017; GENBANK/DQ107018; GENBANK/DQ107019; GENBANK/DQ107020; GENBANK/DQ107021; GENBANK/DQ107022; GENBANK/DQ107023; GENBANK/DQ107024; GENBANK/DQ107025; GENBANK/DQ107026; GENBANK/DQ107027; GENBANK/DQ107028; GENBANK/DQ107029; GENBANK/DQ107030; GENBANK/DQ107031; GENBANK/DQ107032; GENBANK/DQ107033; GENBANK/DQ107034; GENBANK/DQ107035; GENBANK/DQ107036; GENBANK/DQ107037; GENBANK/DQ107038; GENBANK/DQ107039; GENBANK/DQ107040; GENBANK/DQ107041; GENBANK/DQ107042; GENBANK/DQ107043; GENBANK/DQ107044; GENBANK/DQ107045; GENBANK/DQ107046; GENBANK/DQ107047; GENBANK/DQ107048; GENBANK/DQ107049; GENBANK/DQ107050; GENBANK/DQ107051; GENBANK/DQ107052; GENBANK/DQ107053; GENBANK/DQ107054; GENBANK/DQ107055; GENBANK/DQ107056; GENBANK/DQ107057; GENBANK/DQ107058; GENBANK/DQ107059; GENBANK/DQ107060; GENBANK/DQ107061; GENBANK/DQ107062; GENBANK/DQ107063; GENBANK/DQ107064; GENBANK/DQ107065; GENBANK/DQ107066; GENBANK/DQ107067; GENBANK/DQ107068; GENBANK/DQ107069; GENBANK/DQ107070; GENBANK/DQ107071; GENBANK/DQ107072; GENBANK/DQ107073; GENBANK/DQ107074; GENBANK/DQ107075; GENBANK/DQ107076; GENBANK/DQ107077; GENBANK/DQ107078; GENBANK/DQ107079; GENBANK/DQ107080; GENBANK/DQ107081; GENBANK/DQ107082; GENBANK/DQ107083; GENBANK/DQ107084; GENBANK/DQ107085; GENBANK/DQ107086; GENBANK/DQ107087; GENBANK/DQ107088; GENBANK/DQ107089; GENBANK/DQ107090; GENBANK/DQ107091; GENBANK/DQ107092; GENBANK/DQ107093; GENBANK/DQ107094; GENBANK/DQ107095; GENBANK/DQ107096; GENBANK/DQ107097; GENBANK/DQ107098; GENBANK/DQ107099; GENBANK/DQ107100; GENBANK/DQ107101; GENBANK/DQ107102; GENBANK/DQ107103; GENBANK/DQ107104; GENBANK/DQ107105; GENBANK/DQ107106; GENBANK/DQ107107; GENBANK/DQ107108; GENBANK/DQ107109; GENBANK/DQ107110; GENBANK/DQ107111; GENBANK/DQ107112; GENBANK/DQ107113; GENBANK/DQ107114; GENBANK/DQ107115; GENBANK/DQ107116; GENBANK/DQ107117; GENBANK/DQ107118; GENBANK/DQ107119; GENBANK/DQ107120; GENBANK/DQ107121; GENBANK/DQ107122; GENBANK/DQ107123; GENBANK/DQ107124; GENBANK/DQ107125; GENBANK/DQ107126; GENBANK/DQ107127; GENBANK/DQ107128; GENBANK/DQ107129; GENBANK/DQ107130; GENBANK/DQ107131; GENBANK/DQ107132; GENBANK/DQ107133; GENBANK/DQ107134; GENBANK/DQ107135; GENBANK/DQ107136; GENBANK/DQ107137; GENBANK/DQ107138; GENBANK/DQ107139; GENBANK/DQ107140; GENBANK/DQ107141; GENBANK/DQ107142; GENBANK/DQ107143; GENBANK/DQ107144; GENBANK/DQ107145; GENBANK/DQ107146; GENBANK/DQ107147; GENBANK/DQ107148; GENBANK/DQ107149; GENBANK/DQ107150; GENBANK/DQ107151; GENBANK/DQ107152; GENBANK/DQ107153; GENBANK/DQ107154; GENBANK/DQ107155; GENBANK/DQ107156; GENBANK/DQ107157; GENBANK/DQ107158; GENBANK/DQ107159; GENBANK/DQ107160},  So = {Science. 2006 Jan 27;311(5760):538-41.},  Stat = {MEDLINE},  Title = {A virus reveals population structure and recent demographic history of its carnivore host.},  Volume = {311},  Year = {2006 Jan 27},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1121360}}  @article{Edwards:2006fp,  Abstract = {BACKGROUND: Genetic diversity of the human immunodeficiency virus type 1 (HIV-1) population within an individual is lost during transmission to a new host. The demography of transmission is an important determinant of evolutionary dynamics, particularly the relative impact of natural selection and genetic drift immediately following HIV-1 infection. Despite this, the magnitude of this population bottleneck is unclear. RESULTS: We use coalescent methods to quantify the bottleneck in a single case of homosexual transmission and find that over 99% of the env and gag diversity present in the donor is lost. This was consistent with the diversity present at seroconversion in nine other horizontally infected individuals. Furthermore, we estimated viral diversity at birth in 27 infants infected through vertical transmission and found there to be no difference between the two modes of transmission. CONCLUSION: Assuming the bottleneck at transmission is selectively neutral, such a severe reduction in genetic diversity has important implications for adaptation in HIV-1, since beneficial mutations have a reduced chance of transmission.},  Address = {Nuffield Department of Clinical Medicine, University of Oxford, The Peter Medawar Building for Pathogen Research, Oxford, OX1 3SY, UK. [email protected]},  Au = {Edwards, C T and Holmes, E C and Wilson, D J and Viscidi, R P and Abrams, E J and Phillips, R E and Drummond, A J},  Author = {Edwards, Charles T T and Holmes, Edward C and Wilson, Daniel J and Viscidi, Raphael P and Abrams, Elaine J and Phillips, Rodney E and Drummond, Alexei J},  Da = {20060424},  Date-Added = {2008-11-28 10:40:53 -0800},  Date-Modified = {2014-07-06 03:57:25 +0000},  Dcom = {20060721},  Dep = {20060323},  Doi = {10.1186/1471-2148-6-28},  Edat = {2006/03/25 09:00},  Gr = {United Kingdom Wellcome Trust},  Issn = {1471-2148 (Electronic)},  Jid = {100966975},  Journal = {BMC Evol Biol},  Jt = {BMC evolutionary biology},  Language = {eng},  Lr = {20070813},  Mh = {Bayes Theorem; *Disease Transmission, Horizontal; Disease Transmission, Vertical; *Evolution, Molecular; Female; HIV Core Protein p24/genetics; HIV Envelope Protein gp120/genetics; HIV Infections/*transmission/*virology; HIV-1/*genetics; Homosexuality; Humans; Infant, Newborn; Male; Models, Biological; Phylogeny; Time Factors; Variation (Genetics)/*genetics},  Mhda = {2006/07/22 09:00},  Own = {NLM},  Pages = {28},  Phst = {2005/10/04 {$[$}received{$]$}; 2006/03/23 {$[$}accepted{$]$}; 2006/03/23 {$[$}aheadofprint{$]$}},  Pii = {1471-2148-6-28},  Pl = {England},  Pmc = {PMC1444934},  Pmid = {16556318},  Pst = {epublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Electronic},  Rn = {0 (HIV Core Protein p24); 0 (HIV Envelope Protein gp120)},  Sb = {IM},  So = {BMC Evol Biol. 2006 Mar 23;6:28.},  Stat = {MEDLINE},  Title = {Population genetic estimation of the loss of genetic diversity during horizontal transmission of HIV-1.},  Volume = {6},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1186/1471-2148-6-28}}  @article{Edwards:2006eu,  Abstract = {The evolution of the human immunodeficiency virus (HIV-1) during chronic infection involves the rapid, continuous turnover of genetic diversity. However, the role of natural selection, relative to random genetic drift, in governing this process is unclear. We tested a stochastic model of genetic drift using partial envelope sequences sampled longitudinally in 28 infected children. In each case the Bayesian posterior (empirical) distribution of coalescent genealogies was estimated using Markov chain Monte Carlo methods. Posterior predictive simulation was then used to generate a null distribution of genealogies assuming neutrality, with the null and empirical distributions compared using four genealogy-based summary statistics sensitive to nonneutral evolution. Because both null and empirical distributions were generated within a coalescent framework, we were able to explicitly account for the confounding influence of demography. From the distribution of corrected P-values across patients, we conclude that empirical genealogies are more asymmetric than expected if evolution is driven by mutation and genetic drift only, with an excess of low-frequency polymorphisms in the population. This indicates that although drift may still play an important role, natural selection has a strong influence on the evolution of HIV-1 envelope. A negative relationship between effective population size and substitution rate indicates that as the efficacy of selection increases, a smaller proportion of mutations approach fixation in the population. This suggests the presence of deleterious mutations. We therefore conclude that intrahost HIV-1 evolution in envelope is dominated by purifying selection against low-frequency deleterious mutations that do not reach fixation.},  Address = {Nuffield Department of Clinical Medicine, University of Oxford, UK, and Department of Pediatrics, The Johns Hopkins Hospital, Baltimore, MD 21287, USA. [email protected]},  Au = {Edwards, CT and Holmes, EC and Pybus, OG and Wilson, DJ and Viscidi, RP and Abrams, EJ and Phillips, RE and Drummond, AJ},  Author = {Edwards, C T T and Holmes, E C and Pybus, O G and Wilson, D J and Viscidi, R P and Abrams, E J and Phillips, R E and Drummond, A J},  Da = {20061123},  Date-Added = {2008-11-28 10:40:46 -0800},  Date-Modified = {2008-11-28 10:40:46 -0800},  Dcom = {20070131},  Dep = {20060901},  Doi = {10.1534/genetics.105.052019},  Edat = {2006/09/05 09:00},  Gr = {United Kingdom Wellcome Trust},  Issn = {0016-6731 (Print)},  Jid = {0374636},  Journal = {Genetics},  Jt = {Genetics},  Language = {eng},  Lr = {20070813},  Mh = {Base Sequence; Bayes Theorem; Child; Chronic Disease; Computer Simulation; *Evolution, Molecular; Gene Products, env/*genetics; Genes, Viral; *Genetic Drift; HIV Infections/genetics; *HIV-1; Humans; Molecular Sequence Data; Monte Carlo Method; Mutation; Polymorphism, Genetic; *Selection (Genetics); Stochastic Processes},  Mhda = {2007/02/01 09:00},  Number = {3},  Own = {NLM},  Pages = {1441--1453},  Phst = {2006/09/01 {$[$}aheadofprint{$]$}},  Pii = {genetics.105.052019},  Pl = {United States},  Pmc = {PMC1667091},  Pmid = {16951087},  Pst = {ppublish},  Pt = {Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.},  Pubm = {Print-Electronic},  Rn = {0 (Gene Products, env)},  Sb = {IM},  Si = {GENBANK/AY823998; GENBANK/AY823999; GENBANK/AY824000; GENBANK/AY824001; GENBANK/AY824002; GENBANK/AY824003; GENBANK/AY824004; GENBANK/AY824005; GENBANK/AY824006; GENBANK/AY824007; GENBANK/AY824008; GENBANK/AY824009; GENBANK/AY824010; GENBANK/AY824011; GENBANK/AY824012; GENBANK/AY824013; GENBANK/AY824014; GENBANK/AY824015; GENBANK/AY824016; GENBANK/AY824017; GENBANK/AY824018; GENBANK/AY824019; GENBANK/AY824020; GENBANK/AY824021; GENBANK/AY824022; GENBANK/AY824023; GENBANK/AY824024; GENBANK/AY824025; GENBANK/AY824026; GENBANK/AY824027; GENBANK/AY824028; GENBANK/AY824029; GENBANK/AY824030; GENBANK/AY824031; GENBANK/AY824032; GENBANK/AY824033; GENBANK/AY824034; GENBANK/AY824035; GENBANK/AY824036; GENBANK/AY824037; GENBANK/AY824038; GENBANK/AY824039; GENBANK/AY824040; GENBANK/AY824041; GENBANK/AY824042; GENBANK/AY824043; GENBANK/AY824044; 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GENBANK/AY824829; GENBANK/AY824830; GENBANK/AY824831; GENBANK/AY824832; GENBANK/AY824833; GENBANK/AY824834; GENBANK/AY824835; GENBANK/AY824836; GENBANK/AY824837; GENBANK/AY824838; GENBANK/AY824839; GENBANK/AY824840; GENBANK/AY824841; GENBANK/AY824842; GENBANK/AY824843; GENBANK/AY824844; GENBANK/AY824845; GENBANK/AY824846; GENBANK/AY824847; GENBANK/AY824848; GENBANK/AY824849; GENBANK/AY824850; GENBANK/AY824851; GENBANK/AY824852; GENBANK/AY824853; GENBANK/AY824854; GENBANK/AY824855; GENBANK/AY824856; GENBANK/AY824857; GENBANK/AY824858; GENBANK/AY824859; GENBANK/AY824860; GENBANK/AY824861; GENBANK/AY824862; GENBANK/AY824863; GENBANK/AY824864; GENBANK/AY824865; GENBANK/AY824866; GENBANK/AY824867; GENBANK/AY824868; GENBANK/AY824869; GENBANK/AY824870; GENBANK/AY824871; GENBANK/AY824872; GENBANK/AY824873; GENBANK/AY824874; GENBANK/AY824875; GENBANK/AY824876; GENBANK/AY824877; GENBANK/AY824878; GENBANK/AY824879; GENBANK/AY824880; GENBANK/AY824881; GENBANK/AY824882; GENBANK/AY824883; GENBANK/AY824884; GENBANK/AY824885; GENBANK/AY824886; GENBANK/AY824887; GENBANK/AY824888; GENBANK/AY824889; GENBANK/AY824890; GENBANK/AY824891; GENBANK/AY824892; GENBANK/AY824893; GENBANK/AY824894; GENBANK/AY824895; GENBANK/AY824896; GENBANK/AY824897; GENBANK/AY824898; GENBANK/AY824899; GENBANK/AY824900; GENBANK/AY824901; GENBANK/AY824902; GENBANK/AY824903; GENBANK/AY824904; GENBANK/AY824905; GENBANK/AY824906; GENBANK/AY824907; GENBANK/AY824908; GENBANK/AY824909; GENBANK/AY824910; GENBANK/AY824911; GENBANK/AY824912; GENBANK/AY824913; GENBANK/AY824914; GENBANK/AY824915; GENBANK/AY824916; GENBANK/AY824917; GENBANK/AY824918; GENBANK/AY824919; GENBANK/AY824920; GENBANK/AY824921; GENBANK/AY824922; GENBANK/AY824923; GENBANK/AY824924; GENBANK/AY824925; GENBANK/AY824926; GENBANK/AY824927; GENBANK/AY824928; GENBANK/AY824929; GENBANK/AY824930; GENBANK/AY824931; GENBANK/AY824932; GENBANK/AY824933; GENBANK/AY824934; GENBANK/AY824935; GENBANK/AY824936; GENBANK/AY824937; GENBANK/AY824938; GENBANK/AY824939; GENBANK/AY824940; GENBANK/AY824941; GENBANK/AY824942; GENBANK/AY824943; GENBANK/AY824944; GENBANK/AY824945; GENBANK/AY824946},  So = {Genetics. 2006 Nov;174(3):1441-53. Epub 2006 Sep 1.},  Stat = {MEDLINE},  Title = {Evolution of the human immunodeficiency virus envelope gene is dominated by purifying selection.},  Volume = {174},  Year = {2006 Nov},  Bdsk-Url-1 = {http://dx.doi.org/10.1534/genetics.105.052019}}  @article{Pybus:2007fv,  Abstract = {Populations of RNA viruses are often characterized by abundant genetic variation. However, the relative fitness of these mutations is largely unknown, although this information is central to our understanding of viral emergence, immune evasion, and drug resistance. Here we develop a phylogenetic method, based on the distribution of nonsynonymous and synonymous changes, to assess the relative fitness of polymorphisms in the structural genes of 143 RNA viruses. This reveals that a substantial proportion of the amino acid variation observed in natural populations of RNA viruses comprises transient deleterious mutations that are later purged by purifying selection, potentially limiting virus adaptability. We also demonstrate, for the first time, the existence of a relationship between amino acid variability and the phylogenetic distribution of polymorphisms. From this relationship, we propose an empirical threshold for the maximum viable deleterious mutation load in RNA viruses.},  Address = {Department of Zoology, University of Oxford, Oxford, United Kingdom. [email protected]},  Au = {Pybus, OG and Rambaut, A and Belshaw, R and Freckleton, RP and Drummond, AJ and Holmes, EC},  Author = {Pybus, Oliver G and Rambaut, Andrew and Belshaw, Robert and Freckleton, Robert P and Drummond, Alexei J and Holmes, Edward C},  Da = {20070301},  Date-Added = {2008-11-28 10:40:45 -0800},  Date-Modified = {2008-11-28 10:40:45 -0800},  Dcom = {20070823},  Dep = {20070111},  Doi = {10.1093/molbev/msm001},  Edat = {2007/01/16 09:00},  Issn = {0737-4038 (Print)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Mh = {Amino Acid Sequence; Computational Biology; *Evolution, Molecular; Likelihood Functions; Models, Genetic; Mutation/*genetics; *Phylogeny; *Polymorphism, Genetic; RNA Viruses/*genetics; Selection (Genetics)},  Mhda = {2007/08/24 09:00},  Number = {3},  Own = {NLM},  Pages = {845--852},  Phst = {2007/01/11 {$[$}aheadofprint{$]$}},  Pii = {msm001},  Pl = {United States},  Pmid = {17218639},  Pst = {ppublish},  Pt = {Comparative Study; Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Sb = {IM},  So = {Mol Biol Evol. 2007 Mar;24(3):845-52. Epub 2007 Jan 11.},  Stat = {MEDLINE},  Title = {Phylogenetic evidence for deleterious mutation load in RNA viruses and its contribution to viral evolution.},  Volume = {24},  Year = {2007 Mar},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msm001}}  @article{Lemey:2007yg,  Address = {Department of Zoology, University of Oxford, Oxford, United Kingdom. [email protected]},  Au = {Lemey, P and Kosakovsky Pond, SL and Drummond, AJ and Pybus, OG and Shapiro, B and Barroso, H and Taveira, N and Rambaut, A},  Author = {Lemey, Philippe and Kosakovsky Pond, Sergei L and Drummond, Alexei J and Pybus, Oliver G and Shapiro, Beth and Barroso, Helena and Taveira, Nuno and Rambaut, Andrew},  Da = {20070521},  Date-Added = {2008-11-28 10:40:43 -0800},  Date-Modified = {2008-11-28 10:40:43 -0800},  Dcom = {20070619},  Dep = {20070102},  Doi = {10.1371/journal.pcbi.0030029},  Edat = {2007/02/20 09:00},  Gr = {AI36214/AI/United States NIAID; AI43638/AI/United States NIAID; AI47745/AI/United States NIAID; AI57167/AI/United States NIAID; United Kingdom Wellcome Trust},  Issn = {1553-7358 (Electronic)},  Jid = {101238922},  Journal = {PLoS Comput Biol},  Jt = {PLoS computational biology},  Language = {eng},  Lr = {20071114},  Mh = {Amino Acid Sequence; Amino Acid Substitution/*genetics; Codon/genetics; Computer Simulation; DNA Mutational Analysis/methods; Disease Progression; *Evolution, Molecular; Genetic Predisposition to Disease/genetics; HIV Infections/*genetics; Humans; *Models, Genetic; Molecular Sequence Data; Variation (Genetics)/genetics; Viral Envelope Proteins/*genetics; Virus Activation/*genetics; Virus Replication/*genetics},  Mhda = {2007/06/20 09:00},  Number = {2},  Own = {NLM},  Pages = {e29},  Phst = {2006/09/05 {$[$}received{$]$}; 2006/12/29 {$[$}accepted{$]$}; 2007/01/02 {$[$}aheadofprint{$]$}},  Pii = {06-PLCB-RA-0364R2},  Pl = {United States},  Pmc = {PMC1797821},  Pmid = {17305421},  Pst = {ppublish},  Pt = {Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Rn = {0 (Codon); 0 (Viral Envelope Proteins)},  Sb = {IM},  Si = {GENBANK/DQ787116; GENBANK/DQ787117; GENBANK/DQ787118; GENBANK/DQ787119; GENBANK/DQ787120; GENBANK/DQ787121},  So = {PLoS Comput Biol. 2007 Feb 16;3(2):e29. Epub 2007 Jan 2.},  Stat = {MEDLINE},  Title = {Synonymous substitution rates predict HIV disease progression as a result of underlying replication dynamics.},  Volume = {3},  Year = {2007 Feb 16},  Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pcbi.0030029}}  @article{Ho:2007zl,  Address = {Department of Zoology, University of Oxford, Oxford, United Kingdom. [email protected]},  Au = {Ho, SY and Shapiro, B and Phillips, MJ and Cooper, A and Drummond, AJ},  Author = {Ho, Simon Y W and Shapiro, Beth and Phillips, Matthew J and Cooper, Alan and Drummond, Alexei J},  Da = {20070612},  Date-Added = {2008-11-28 10:40:40 -0800},  Date-Modified = {2008-11-28 10:40:40 -0800},  Dcom = {20070913},  Doi = {10.1080/10635150701435401},  Edat = {2007/06/15 09:00},  Issn = {1063-5157 (Print)},  Jid = {9302532},  Journal = {Syst Biol},  Jt = {Systematic biology},  Language = {eng},  Mh = {Animals; Bison/classification; Computational Biology/*methods; *Evolution, Molecular; Humans; Time Factors},  Mhda = {2007/09/14 09:00},  Number = {3},  Own = {NLM},  Pages = {515--522},  Pii = {779485199},  Pl = {England},  Pmid = {17562475},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print},  Sb = {IM},  So = {Syst Biol. 2007 Jun;56(3):515-22.},  Stat = {MEDLINE},  Title = {Evidence for time dependency of molecular rate estimates.},  Volume = {56},  Year = {2007 Jun},  Bdsk-Url-1 = {http://dx.doi.org/10.1080/10635150701435401}}  @article{Holmes:2007rm,  Abstract = {Despite the wealth of data describing the ecological factors that underpin viral emergence, little is known about the evolutionary processes that allow viruses to jump species barriers and establish productive infections in new hosts. Understanding the evolutionary basis to virus emergence is therefore a key research goal and many of the debates in this area can be considered within the rigorous theoretical framework established by evolutionary genetics. In particular, the respective roles played by natural selection and genetic drift in shaping genetic diversity are also of fundamental importance for understanding the nature of viral emergence. Herein, we discuss whether there are evolutionary rules to viral emergence, and especially whether certain types of virus, or those that infect a particular type of host species, are more likely to emerge than others. We stress the complex interplay between rates of viral evolution and the ability to recognize cell receptors from phylogenetically divergent host species. We also emphasize the current lack of convincing data as to whether viral emergence requires adaptation to the new host species during the early stages of infection, or whether it is largely a chance process involving the transmission of a viral strain with the necessary genetic characteristics.},  Address = {Center for Infectious Disease Dynamics, Department of Biology, Mueller Laboratory, The Pennsylvania State University, University Park, PA 16802, USA. [email protected]},  Au = {Holmes, EC and Drummond, AJ},  Author = {Holmes, E C and Drummond, A J},  Da = {20070912},  Date-Added = {2008-11-28 10:40:34 -0800},  Date-Modified = {2008-11-28 10:40:34 -0800},  Dcom = {20070927},  Edat = {2007/09/13 09:00},  Gr = {United Kingdom Wellcome Trust},  Issn = {0070-217X (Print)},  Jid = {0110513},  Journal = {Curr Top Microbiol Immunol},  Jt = {Current topics in microbiology and immunology},  Language = {eng},  Mh = {Adaptation, Physiological; Animals; Communicable Diseases, Emerging/transmission/*veterinary/virology; *Evolution, Molecular; Humans; Recombination, Genetic; Species Specificity; Viral Physiology; Virus Diseases/*transmission/*veterinary/virology; Viruses/*genetics; *Zoonoses},  Mhda = {2007/09/28 09:00},  Own = {NLM},  Pages = {51--66},  Pl = {Germany},  Pmid = {17848060},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't; Review},  Pubm = {Print},  Rf = {53},  Sb = {IM},  So = {Curr Top Microbiol Immunol. 2007;315:51-66.},  Stat = {MEDLINE},  Title = {The evolutionary genetics of viral emergence.},  Volume = {315},  Year = {2007}}  @article{Rambaut:2008rz,  Abstract = {DNA sequences extracted from ancient remains are increasingly used to generate large population data sets, often spanning tens of thousands of years of population history. Bayesian coalescent methods such as those implemented in the software package BEAST can be used to estimate the demographic history of these populations, sometimes resulting in complex scenarios of fluctuations in population size, which can be correlated with the timing of environmental events, such as glaciations. Recently, however, Axelsson et al. (2008) claimed that many of these complex demographic trends are likely to be the result of post-mortem DNA damage, a problem that they investigate by removing all sites involving transitions from ancient sequences prior to analysis. When this solution is applied to a previously published data set of Pleistocene bison, they show that the demographic signal of population expansion and decline disappears. While some apparently segregating mutations in ancient sequences may be due to post-mortem damage, we argue that discarding the data will result in loss of power to detect patterns of population change. Instead, to accommodate this problem, we implement a model in which sequences are the result of a joint process of molecular evolution and post-mortem DNA damage within a probabilistic inference framework. Through simulation, we demonstrate the ability of this model to accurately recover evolutionary parameters, demographic history and DNA damage rates. When this model is applied to the bison data set, we find that the rate of DNA damage is significant but low, and that the reconstruction of population size history is nearly identical to previously published estimates.},  Address = {Institute of Evolutionary Biology, University of Edinburgh, King's Buildings, Edinburgh, EH9 3JT, UK.},  Author = {Rambaut, A and Ho, S. Y. W. and Drummond, A. J. and Shapiro, B},  Da = {20081112},  Date-Added = {2008-11-28 10:40:27 -0800},  Date-Modified = {2014-07-06 00:54:27 +0000},  Dep = {20081111},  Doi = {10.1093/molbev/msn256},  Edat = {2008/11/13 09:00},  Issn = {1537-1719 (Electronic)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {ENG},  Mhda = {2008/11/13 09:00},  Own = {NLM},  Pii = {msn256},  Pmid = {19001634},  Pst = {aheadofprint},  Pt = {JOURNAL ARTICLE},  Pubm = {Print-Electronic},  So = {Mol Biol Evol. 2008 Nov 11.},  Stat = {Publisher},  Title = {Accommodating the effect of ancient DNA damage on inferences of demographic histories.},  Year = {2008 Nov 11},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msn256}}  @article{Atkinson:2008nr,  Abstract = {Past population size can be estimated from modern genetic diversity using coalescent theory. Estimates of ancestral human population dynamics in sub-Saharan Africa can tell us about the timing and nature of our first steps towards colonizing the globe. Here, we combine Bayesian coalescent inference with a dataset of 224 complete human mitochondrial DNA (mtDNA) sequences to estimate effective population size through time for each of the four major African mtDNA haplogroups (L0-L3). We find evidence of three distinct demographic histories underlying the four haplogroups. Haplogroups L0 and L1 both show slow, steady exponential growth from 156 to 213kyr ago. By contrast, haplogroups L2 and L3 show evidence of substantial growth beginning 12-20 and 61-86kyr ago, respectively. These later expansions may be associated with contemporaneous environmental and/or cultural changes. The timing of the L3 expansion-8-12kyr prior to the emergence of the first non-African mtDNA lineages-together with high L3 diversity in eastern Africa, strongly supports the proposal that the human exodus from Africa and subsequent colonization of the globe was prefaced by a major expansion within Africa, perhaps driven by some form of cultural innovation.},  Address = {Institute of Cognitive and Evolutionary Anthropology, University of Oxford, 64 Banbury Road, Oxford OX2 6PN, UK.},  Author = {Atkinson, Q. D. and Gray, R. D. and Drummond, A. J.},  Da = {20081001},  Date-Added = {2008-11-28 10:40:25 -0800},  Date-Modified = {2014-07-06 00:53:55 +0000},  Dep = {20080930},  Doi = {10.1098/rspb.2008.0785},  Edat = {2008/10/02 09:00},  Issn = {0962-8452 (Print)},  Jid = {101245157},  Journal = {Proc Biol Sci},  Jt = {Proceedings. Biological sciences / The Royal Society},  Language = {ENG},  Mhda = {2008/10/02 09:00},  Own = {NLM},  Pii = {Q322007083Q68417},  Pmid = {18826938},  Pst = {aheadofprint},  Pt = {JOURNAL ARTICLE},  Pubm = {Print-Electronic},  So = {Proc Biol Sci. 2008 Sep 30.},  Stat = {Publisher},  Title = {Bayesian coalescent inference of major human mitochondrial DNA haplogroup expansions in Africa.},  Year = {2008 Sep 30},  Bdsk-Url-1 = {http://dx.doi.org/10.1098/rspb.2008.0785}}  @article{Atkinson:2008qv,  Abstract = {The relative timing and size of regional human population growth following our expansion from Africa remain unknown. Human mitochondrial DNA (mtDNA) diversity carries a legacy of our population history. Given a set of sequences, we can use coalescent theory to estimate past population size through time and draw inferences about human population history. However, recent work has challenged the validity of using mtDNA diversity to infer species population sizes. Here we use Bayesian coalescent inference methods, together with a global data set of 357 human mtDNA coding-region sequences, to infer human population sizes through time across 8 major geographic regions. Our estimates of relative population sizes show remarkable concordance with the contemporary regional distribution of humans across Africa, Eurasia, and the Americas, indicating that mtDNA diversity is a good predictor of population size in humans. Plots of population size through time show slow growth in sub-Saharan Africa beginning 143-193 kya, followed by a rapid expansion into Eurasia after the emergence of the first non-African mtDNA lineages 50-70 kya. Outside Africa, the earliest and fastest growth is inferred in Southern Asia approximately 52 kya, followed by a succession of growth phases in Northern and Central Asia (approximately 49 kya), Australia (approximately 48 kya), Europe (approximately 42 kya), the Middle East and North Africa (approximately 40 kya), New Guinea (approximately 39 kya), the Americas (approximately 18 kya), and a second expansion in Europe (approximately 10-15 kya). Comparisons of relative regional population sizes through time suggest that between approximately 45 and 20 kya most of humanity lived in Southern Asia. These findings not only support the use of mtDNA data for estimating human population size but also provide a unique picture of human prehistory and demonstrate the importance of Southern Asia to our recent evolutionary past.},  Address = {Institute of Cognitive and Evolutionary Anthropology, University of Oxford, 58A Banbury Rd, Oxford, OX2 6QS, United Kingdom. [email protected]},  Au = {Atkinson, QD and Gray, RD and Drummond, AJ},  Author = {Atkinson, Quentin D and Gray, Russell D and Drummond, Alexei J},  Da = {20080206},  Date-Added = {2008-11-28 10:40:24 -0800},  Date-Modified = {2008-11-28 10:40:24 -0800},  Dcom = {20080519},  Dep = {20071218},  Doi = {10.1093/molbev/msm277},  Edat = {2007/12/21 09:00},  Issn = {1537-1719 (Electronic)},  Jid = {8501455},  Journal = {Mol Biol Evol},  Jt = {Molecular biology and evolution},  Language = {eng},  Mh = {Asia; Bayes Theorem; DNA, Mitochondrial/*genetics; *Genetics, Population; Humans; *Population Density; *Variation (Genetics)},  Mhda = {2008/05/20 09:00},  Number = {2},  Own = {NLM},  Pages = {468--474},  Phst = {2007/12/18 {$[$}aheadofprint{$]$}; 2008/01/03 {$[$}aheadofprint{$]$}},  Pii = {msm277},  Pl = {United States},  Pmid = {18093996},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Rn = {0 (DNA, Mitochondrial)},  Sb = {IM},  So = {Mol Biol Evol. 2008 Feb;25(2):468-74. Epub 2007 Dec 18.},  Stat = {MEDLINE},  Title = {mtDNA variation predicts population size in humans and reveals a major Southern Asian chapter in human prehistory.},  Volume = {25},  Year = {2008 Feb},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msm277}}  @article{Hon:2008xy,  Abstract = {Bats have been identified as the natural reservoir of severe acute respiratory syndrome (SARS)-like and SARS coronaviruses (SLCoV and SCoV). However, previous studies suggested that none of the currently sampled bat SLCoVs is the descendant of the direct ancestor of SCoV, based on their relatively distant phylogenetic relationship. In this study, evidence of the recombinant origin of the genome of a bat SLCoV is demonstrated. We identified a potential recombination breakpoint immediately after the consensus intergenic sequence between open reading frame 1 and the S coding region, suggesting the replication intermediates may participate in the recombination event, as previously speculated for other CoVs. Phylogenetic analysis of its parental regions suggests the presence of an uncharacterized SLCoV lineage that is phylogenetically closer to SCoVs than any of the currently sampled bat SLCoVs. Using various Bayesian molecular-clock models, interspecies transfer of this SLCoV lineage from bats to the amplifying host (e.g., civets) was estimated to have happened a median of 4.08 years before the SARS outbreak. Based on this relatively short window period, we speculate that this uncharacterized SLCoV lineage may contain the direct ancestor of SCoV. This study sheds light on the possible host bat species of the direct ancestor of SCoV, providing valuable information on the scope and focus of surveillance for the origin of SCoV.},  Address = {5N-12, Kadoorie Biological Science Building, The University of Hong Kong, Hong Kong, China.},  Au = {Hon, CC and Lam, TY and Shi, ZL and Drummond, AJ and Yip, CW and Zeng, F and Lam, PY and Leung, FC},  Author = {Hon, Chung-Chau and Lam, Tsan-Yuk and Shi, Zheng-Li and Drummond, Alexei J and Yip, Chi-Wai and Zeng, Fanya and Lam, Pui-Yi and Leung, Frederick Chi-Ching},  Da = {20080131},  Date-Added = {2008-11-28 10:40:24 -0800},  Date-Modified = {2008-11-28 10:40:24 -0800},  Dcom = {20080305},  Dep = {20071205},  Doi = {10.1128/JVI.01926-07},  Edat = {2007/12/07 09:00},  Issn = {1098-5514 (Electronic)},  Jid = {0113724},  Journal = {J Virol},  Jt = {Journal of virology},  Language = {eng},  Mh = {Animals; Base Sequence; Bayes Theorem; Chiroptera/*virology; Genome, Viral/*genetics; *Models, Genetic; Molecular Sequence Data; Phylogeny; Recombination, Genetic; SARS Virus/*classification/*genetics/isolation \& purification},  Mhda = {2008/03/06 09:00},  Number = {4},  Own = {NLM},  Pages = {1819--1826},  Phst = {2007/12/05 {$[$}aheadofprint{$]$}},  Pii = {JVI.01926-07},  Pl = {United States},  Pmc = {PMC2258724},  Pmid = {18057240},  Pst = {ppublish},  Pt = {Journal Article; Research Support, Non-U.S. Gov't},  Pubm = {Print-Electronic},  Sb = {IM},  So = {J Virol. 2008 Feb;82(4):1819-26. Epub 2007 Dec 5.},  Stat = {MEDLINE},  Title = {Evidence of the recombinant origin of a bat severe acute respiratory syndrome (SARS)-like coronavirus and its implications on the direct ancestor of SARS coronavirus.},  Volume = {82},  Year = {2008 Feb},  Bdsk-Url-1 = {http://dx.doi.org/10.1128/JVI.01926-07}}  @article{treeviz,  Author = {Hillis, D.M. and Heath, T.A. and St John, K.},  Journal = {Systematic Biology},  Number = {3},  Pages = {471-82},  Title = {Analysis and Visualization of Tree Space},  Volume = {54},  Year = {2005}}  @incollection{bryant2003,  Added-At = {2009-01-28T01:17:14.000+0100},  Address = {Providence, RI},  Author = {Bryant, David},  Biburl = {http://www.bibsonomy.org/bibtex/221aa009b601dcdb642893c96da9b98ef/compevol},  Booktitle = {Bioconsensus ({P}iscataway, {NJ}, 2000/2001)},  Date-Added = {2009-01-28 12:07:05 +1300},  Date-Modified = {2009-01-28 13:04:38 +1300},  Interhash = {084b5b31a5f89e171dc2a85942abd28b},  Intrahash = {21aa009b601dcdb642893c96da9b98ef},  Keywords = {from:davidjamesbryant},  Mrclass = {92B10 (05C05 91B12 92D15)},  Mrnumber = {MR1982426 (2004f:92002)},  Pages = {163--183},  Publisher = {Amer. Math. Soc.},  Series = {DIMACS Ser. Discrete Math. Theoret. Comput. Sci.},  Title = {A classification of consensus methods for phylogenetics},  Volume = 61,  Year = 2003}  @article{SplitsTree,  Author = {Huson, D. H. and Bryant, D.},  Doi = {10.1093/molbev/msj030},  Journal = {Mol. Biol. Evol.},  Number = {2},  Pages = {254--267},  Title = {Application of Phylogenetic Networks in Evolutionary Studies},  Volume = {23},  Year = {2006},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/molbev/msj030}}  @article{jackman1999,  Author = {Jackman, T. and Larson, A. and Queiroz, K. De and Losos, J.},  Journal = {Systematic Biology},  Number = {2},  Pages = {254-285},  Title = {Phylogenetic relationships and tempo of early diversification in Anolis lizards},  Volume = {48},  Year = {1999}}  @article{wiens2008,  Author = {Wiens, John J. and Moen, Daniel S.},  Doi = {DOI: 10.3724/SP.J.1002.2008.08040},  Journal = {Journal of Systematics and Evolution},  Number = {3},  Pages = {307-314},  Title = {Missing data and the accuracy of Bayesian phylogenetics},  Volume = {46},  Year = {2008},  Bdsk-Url-1 = {http://dx.doi.org/10.3724/SP.J.1002.2008.08040}}  @article{rosenbergSK2003,  Author = {Rosenberg, M. S. and Subramanian, S and Kumar, S},  Date-Modified = {2014-12-04 01:13:04 +0000},  Journal = {Mol Biol Evol},  Number = {6},  Pages = {988-93},  Title = {Patterns of transitional mutation biases within and among mammalian genomes},  Volume = {20},  Year = {2003}}  @article{yangY1999,  Author = {Yang, Z. and Yoder, A.D.},  Issue = {3},  Journal = {Journal of Molecular Evolution},  Pages = {274-283},  Title = {Estimation of the transition/transversion rate bias and species sampling},  Volume = {48},  Year = {1999}}  @book{TAOC,  Author = {Knuth, Donald},  Publisher = {Addison-Wesley},  Title = {The Art of Computer Programming. Vol. 2: Seminumerical algorithms},  Year = {1997}}  @article{MatsumotoN1998,  Author = {Matsumoto, M. and Nishimura, T.},  Journal = {ACM Transactions on Modeling and Computer Simulation},  Month = {January},  Number = {1},  Pages = {3--30},  Title = {Mersenne Twister: A 623-Dimensionally Equidistributed Uniform Pseudo-Random Number Generator},  Volume = {8},  Year = {1998}}  @article{BaeleEtAl2012,  Author = {Baele, G. and Lemey, P. and Bedford, T. and Rambaut, A. and Suchard, M. A. and Alekseyenko, A. V.},  Journal = {Mol. Biol. Evol.},  Number = {9},  Pages = {2157-2167},  Title = {Improving the accuracy of demographic and molecular clock model comparison while accommodating phylogenetic uncertainty},  Volume = {29},  Year = {2012}}  @article{Steel2005,  Author = {Steel, M.},  Journal = {Trends in Genetics},  Number = {6},  Pages = {307-309},  Title = {Should phylogenetic models be trying to 'fit an elephant'?},  Volume = {21},  Year = {2005}}  @article{SNAPP,  Author = {Bryant, David and Bouckaert, Remco R. and Felsenstein, Joseph and Rosenberg, Noah and RoyChoudhury, Arindam},  Date-Modified = {2014-07-06 03:46:27 +0000},  Journal = {Mol. Biol. Evol.},  Number = {8},  Pages = {1917-1932},  Title = {Inferring Species Trees Directly from Biallelic Genetic Markers: Bypassing Gene Trees in a Full Coalescent Analysis},  Volume = {29},  Year = {2012}}  @article{CIR,  Author = {Cox, J.C. and Ingersoll, J.E. and Ross, S.A.},  Journal = {Econometrica},  Pages = {385--407},  Title = {A Theory of the Term Structure of Interest Rates},  Volume = {53},  Year = {1985}}  @incollection{Raftery2007,  Author = {Raftery, A. E. and Newton, M. A. and Satagopan, J and Krivitsky, P},  Booktitle = {Bayesian Statistics},  Date-Modified = {2014-12-04 01:11:27 +0000},  Editor = {Bernardo JM, Bayarri MJ, Berger JO},  Pages = {1--45},  Publisher = {Oxford: Oxford University Press},  Title = {Estimating the integrated likelihood via posterior simulation using the harmonic mean identity},  Year = {2007}}  @article{Xie2011,  Author = {Xie, W and Lewis, PO and Fan, Y and Kuo, L and Chen, MH},  Journal = {Syst Biol},  Pages = {150--160},  Title = {Improving marginal likelihood estimation for Bayesian phylogenetic model selection},  Volume = {60},  Year = {2011}}  @article{densitree,  Author = {Bouckaert, Remco R.},  Doi = {10.1093/bioinformatics/btq110},  Journal = {Bioinformatics},  Number = {10},  Pages = {1372-1373},  Title = {DensiTree: making sense of sets of phylogenetic trees},  Volume = {26},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1093/bioinformatics/btq110}}  @article{Bouckaert2012,  Author = {Bouckaert, Remco R. and Lemey, Philippe and Dunn, Michael and Greenhill, Simon J. and Alekseyenko, Alexander V. and Drummond, Alexei J. and Gray, Russell D. and Suchard, Marc A. and Atkinson, Quentin D.},  Date-Modified = {2014-07-06 00:50:24 +0000},  Doi = {DOI: 10.1126/science.1219669},  Journal = {Science},  Number = {6097},  Pages = {957-960},  Title = {Mapping the Origins and Expansion of the Indo-European Language Family},  Volume = {337},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1126/science.1219669}}  @article{Heled2013,  Author = {Heled, Joseph and Bouckaert, Remco R},  Journal = {BMC evolutionary biology},  Number = {1},  Pages = {221},  Publisher = {BioMed Central Ltd},  Title = {Looking for trees in the forest: summary tree from posterior samples},  Volume = {13},  Year = {2013}}  @article{RGTSNAPP,  Author = {Bouckaert, Remco R. and Bryant, David},  Date-Modified = {2014-07-05 10:31:14 +0000},  Journal = {Available from BEAST 2 wiki},  Title = {A rough guide to SNAPP},  Year = {2012}}  @article{beagle2,  Author = {Ayres, D and Darling, A and Zwickl, D and Beerli, P and Holder, M and Lewis, P and Huelsenbeck, J. P. and Ronquist, F and Swofford, D. L. and Cummings, M. P. and Rambaut, A and Suchard, M. A.},  Date-Modified = {2014-07-06 02:04:20 +0000},  Journal = {Syst Biol},  Pages = {170-173},  Title = {BEAGLE: a common application programming inferface and high-performance computing library for statistical phylogenetics},  Volume = {61},  Year = {2012}}  @article{finches,  Author = {Sato, A. and O'hUigin, C. and Figueroa, F. and Grant, P. R. and Grant, B. R. and Tichy, H. and Klein, J.},  Journal = {Proc. Natl. Acad. Sci},  Pages = {5101--5106},  Title = {Phylogeny of Darwin's finches as revealed by mtDNA sequences},  Volume = {96},  Year = {1999}}  @article{RBmodel,  Author = {Bouckaert, Remco R. and Alvarado-Mora, M\'onica and Rebello Pinho, Jo\~ao},  Date-Modified = {2014-07-06 03:46:34 +0000},  Journal = {Antiviral therapy},  Title = {Evolutionary rates and HBV: issues of rate estimation with Bayesian molecular methods},  Year = {2013}}  @article{clustal,  Author = {Larkin, M.A. and Blackshields, G. and Brown, N.P. and Chenna, R. and McGettigan, P.A. and McWilliam, H. and Valentin, F. and Wallace, I.M. and Wilm, A. and Lopez, R. and Thompson, J.D. and Gibson, T.J. and Higgins, D.G.},  Journal = {Bioinformatics},  Pages = {2947-2948},  Title = {Clustal W and Clustal X version 2.0},  Volume = {23},  Year = {2007}}  @article{deSilva2012inf,  Abstract = {Using sequence data to infer population dynamics is playing an increasing role in the analysis of outbreaks. The most common methods in use, based on coalescent inference, have been widely used but not extensively tested against simulated epidemics. Here, we use simulated data to test the ability of both parametric and non-parametric methods for inference of effective population size (coded in the popular BEAST package) to reconstruct epidemic dynamics. We consider a range of simulations centred on scenarios considered plausible for pandemic influenza, but our conclusions are generic for any exponentially growing epidemic. We highlight systematic biases in non-parametric effective population size estimation. The most prominent such bias leads to the false inference of slowing of epidemic spread in the recent past even when the real epidemic is growing exponentially. We suggest some sampling strategies that could reduce (but not eliminate) some of the biases. Parametric methods can correct for these biases if the infected population size is large. We also explore how some poor sampling strategies (e.g. that over-represent epidemiologically linked clusters of cases) could dramatically exacerbate bias in an uncontrolled manner. Finally, we present a simple diagnostic indicator, based on coalescent density and which can easily be applied to reconstructed phylogenies, that identifies time-periods for which effective population size estimates are less likely to be biased. We illustrate this with an application to the 2009 H1N1 pandemic. },  Author = {de Silva, E. and Ferguson, N.M. and Fraser, C.},  Journal = {J R Soc Interface},  Number = {73},  Pages = {1797-808},  Title = {Inferring pandemic growth rates from sequence data},  Volume = {9},  Year = {2012}}  @article{suchardRed2006,  Author = {Suchard, M A and Redelings, B D},  Date-Modified = {2013-02-13 03:45:18 +0000},  Journal = {Bioinformatics},  Number = {16},  Pages = {2047-2048},  Title = {BAli-Phy: simultaneous Bayesian inference of alignment and phylogeny},  Volume = {22},  Year = {2006}}  @article{RedelingsSuchard2005,  Author = {Redelings, B. D. and Suchard, M. A.},  Date-Modified = {2014-07-06 02:06:20 +0000},  Journal = {Systematic Biology},  Number = {3},  Pages = {401-418},  Title = {Joint Bayesian Estimation of Alignment and Phylogeny},  Volume = {54},  Year = {2005}}  @article{Notredame2000205,  Author = {Notredame, C{\'e}dric and Higgins, Desmond G and Heringa, Jaap},  Doi = {10.1006/jmbi.2000.4042},  Issn = {0022-2836},  Journal = {Journal of Molecular Biology},  Keywords = {multiple sequence alignment},  Number = {1},  Pages = {205 - 217},  Title = {T-coffee: a novel method for fast and accurate multiple sequence alignment},  Url = {http://www.sciencedirect.com/science/article/pii/S0022283600940427},  Volume = {302},  Year = {2000},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S0022283600940427},  Bdsk-Url-2 = {http://dx.doi.org/10.1006/jmbi.2000.4042}}  @book{mcmcHandBook,  Author = {Brooks, Steve and Gelman, Andrew and Jones, Galin L. and Meng, Xiao-Li},  Publisher = {Chapman \& Hall/CRC.},  Title = {Handbook of Markov Chain Monte Carlo},  Year = {2010}}  @article{Hailer20042012,  Abstract = {Recent studies have shown that the polar bear matriline (mitochondrial DNA) evolved from a brown bear lineage since the late Pleistocene, potentially indicating rapid speciation and adaption to arctic conditions. Here, we present a high-resolution data set from multiple independent loci across the nuclear genomes of a broad sample of polar, brown, and black bears. Bayesian coalescent analyses place polar bears outside the brown bear clade and date the divergence much earlier, in the middle Pleistocene, about 600 (338 to 934) thousand years ago. This provides more time for polar bear evolution and confirms previous suggestions that polar bears carry introgressed brown bear mitochondrial DNA due to past hybridization. Our results highlight that multilocus genomic analyses are crucial for an accurate understanding of evolutionary history.},  Author = {Hailer, Frank and Kutschera, Verena E. and Hallstr{\"o}m, Bj{\"o}rn M. and Klassert, Denise and Fain, Steven R. and Leonard, Jennifer A. and Arnason, Ulfur and Janke, Axel},  Doi = {10.1126/science.1216424},  Eprint = {http://www.sciencemag.org/content/336/6079/344.full.pdf},  Journal = {Science},  Number = {6079},  Pages = {344-347},  Title = {Nuclear Genomic Sequences Reveal that Polar Bears Are an Old and Distinct Bear Lineage},  Url = {http://www.sciencemag.org/content/336/6079/344.abstract},  Volume = {336},  Year = {2012},  Bdsk-Url-1 = {http://www.sciencemag.org/content/336/6079/344.abstract},  Bdsk-Url-2 = {http://dx.doi.org/10.1126/science.1216424}}  @article{Molina17052011,  Abstract = {Asian rice, Oryza sativa, is one of world's oldest and most important crop species. Rice is believed to have been domesticated ∼9,000 y ago, although debate on its origin remains contentious. A single-origin model suggests that two main subspecies of Asian rice, indica and japonica, were domesticated from the wild rice O. rufipogon. In contrast, the multiple independent domestication model proposes that these two major rice types were domesticated separately and in different parts of the species range of wild rice. This latter view has gained much support from the observation of strong genetic differentiation between indica and japonica as well as several phylogenetic studies of rice domestication. We reexamine the evolutionary history of domesticated rice by resequencing 630 gene fragments on chromosomes 8, 10, and 12 from a diverse set of wild and domesticated rice accessions. Using patterns of SNPs, we identify 20 putative selective sweeps on these chromosomes in cultivated rice. Demographic modeling based on these SNP data and a diffusion-based approach provide the strongest support for a single domestication origin of rice. Bayesian phylogenetic analyses implementing the multispecies coalescent and using previously published phylogenetic sequence datasets also point to a single origin of Asian domesticated rice. Finally, we date the origin of domestication at ∼8,200--13,500 y ago, depending on the molecular clock estimate that is used, which is consistent with known archaeological data that suggests rice was first cultivated at around this time in the Yangtze Valley of China.},  Author = {Molina, Jeanmaire and Sikora, Martin and Garud, Nandita and Flowers, Jonathan M. and Rubinstein, Samara and Reynolds, Andy and Huang, Pu and Jackson, Scott and Schaal, Barbara A. and Bustamante, Carlos D. and Boyko, Adam R. and Purugganan, Michael D.},  Doi = {10.1073/pnas.1104686108},  Eprint = {http://www.pnas.org/content/108/20/8351.full.pdf+html},  Journal = {Proceedings of the National Academy of Sciences},  Number = {20},  Pages = {8351-8356},  Title = {Molecular evidence for a single evolutionary origin of domesticated rice},  Url = {http://www.pnas.org/content/108/20/8351.abstract},  Volume = {108},  Year = {2011},  Bdsk-Url-1 = {http://www.pnas.org/content/108/20/8351.abstract},  Bdsk-Url-2 = {http://dx.doi.org/10.1073/pnas.1104686108}}  @article{StarBeastApp2010,  Author = {Leach{\'e}, Adam D. and Fujita, Matthew K.},  Date-Modified = {2014-07-07 01:27:07 +0000},  Journal = {Proc R Soc B},  Pages = {3071-3077},  Title = {Bayesian species delimitation in West African forest geckos (Hemidactylus fasciatus)},  Volume = {277},  Year = {2010}}  @article{StarBeastApp2011,  Author = {Dinc{\u a}, Vlad and Lukhtanov, Vladimir A and Talavera, Gerard and Vila, Roger},  Journal = {Nature Communications},  Number = {324},  Title = {Unexpected layers of cryptic diversity in wood white Leptidea butterflies},  Volume = {2},  Year = {2011}}  @article{EVO:EVO1097,  Author = {McCormack, John E. and Heled, Joseph and Delaney, Kathleen S. and Peterson, A. Townsend and Knowles, L. Lacey},  Date-Modified = {2014-07-04 01:47:17 +0000},  Doi = {10.1111/j.1558-5646.2010.01097.x},  Issn = {1558-5646},  Journal = {Evolution},  Keywords = {Aphelocoma, BEAST, divergence times, fossil calibration, gene tree, glaciations, mountain uplift, Pleistocene, species tree},  Number = {1},  Pages = {184--202},  Publisher = {Blackwell Publishing Inc},  Title = {Calibrating Divergence Times On Species Trees Versus Gene Trees: Implications For Speciation History Of Aphelocoma Jays},  Url = {http://dx.doi.org/10.1111/j.1558-5646.2010.01097.x},  Volume = {65},  Year = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1558-5646.2010.01097.x}}  @article{Chaves2011207,  Author = {Chaves, Jaime A. and Smith, Thomas B.},  Date-Modified = {2014-07-05 08:48:09 +0000},  Doi = {10.1016/j.ympev.2011.04.007},  Issn = {1055-7903},  Journal = {Molecular Phylogenetics and Evolution},  Keywords = {Remote sensing},  Number = {2},  Pages = {207 - 218},  Title = {Evolutionary patterns of diversification in the Andean hummingbird genus Adelomyia},  Url = {http://www.sciencedirect.com/science/article/pii/S1055790311001916},  Volume = {60},  Year = {2011},  Bdsk-Url-1 = {http://www.sciencedirect.com/science/article/pii/S1055790311001916},  Bdsk-Url-2 = {http://dx.doi.org/10.1016/j.ympev.2011.04.007}}  @article{DensiTreeApp2011,  Author = {Levinson, Stephen C. and Greenhill, Simon J. and Gray, Russell D. and Dunn, Michael},  Doi = {doi:10.1515/lity.2011.034},  Journal = {Linguistic Typology},  Number = {2},  Pages = {509-534},  Title = {Universal typological dependencies should be detectable in the history of language families},  Volume = {15},  Yar = {2011},  Bdsk-Url-1 = {http://dx.doi.org/10.1515/lity.2011.034}}  @article{PhyloGeoApp2013,  Author = {He, Miao and Miyajima, Fabio and Roberts, Paul and Ellison, Louise and Pickard, Derek J and Martin, Melissa J and Connor, Thomas R and Harris, Simon R and Fairley, Derek and Bamford, Kathleen B and D'Arc, Stephanie and Brazier, Jon and Brown, Derek and Coia, John E and Douce, Gill and Gerding, Dale and Kim, Hee Jung and Koh, Tse Hsien and Kato, Haru and Senoh, Mitsutoshi and Louie, Tom and Michell, Stephen and Butt, Emma and Peacock, Sharon J and Brown, Nick M and Riley, Tom and Songer, Glen and Wilcox, Mark and Pirmohamed, Munir and Kuijper, Ed and Hawkey, Peter and Wren, Brendan W and Dougan, Gordon and Parkhill, Julian and Lawley, Trevor D},  Doi = {http://dx.doi.org/10.1038/ng.2478},  Journal = {Nature Genetics},  Number = {1},  Pages = {109--113},  Title = {Emergence and global spread of epidemic healthcare-associated Clostridium difficile},  Volume = {45},  Year = {2013},  Bdsk-Url-1 = {http://dx.doi.org/10.1038/ng.2478}}  @article{Campos23032010,  Abstract = {The causes of the late Pleistocene megafaunal extinctions are poorly understood. Different lines of evidence point to climate change, the arrival of humans, or a combination of these events as the trigger. Although many species went extinct, others, such as caribou and bison, survived to the present. The musk ox has an intermediate story: relatively abundant during the Pleistocene, it is now restricted to Greenland and the Arctic Archipelago. In this study, we use ancient DNA sequences, temporally unbiased summary statistics, and Bayesian analytical techniques to infer musk ox population dynamics throughout the late Pleistocene and Holocene. Our results reveal that musk ox genetic diversity was much higher during the Pleistocene than at present, and has undergone several expansions and contractions over the past 60,000 years. Northeast Siberia was of key importance, as it was the geographic origin of all samples studied and held a large diverse population until local extinction at ≈45,000 radiocarbon years before present (14C YBP). Subsequently, musk ox genetic diversity reincreased at ca. 30,000 14C YBP, recontracted at ca. 18,000 14C YBP, and finally recovered in the middle Holocene. The arrival of humans into relevant areas of the musk ox range did not affect their mitochondrial diversity, and both musk ox and humans expanded into Greenland concomitantly. Thus, their population dynamics are better explained by a nonanthropogenic cause (for example, environmental change), a hypothesis supported by historic observations on the sensitivity of the species to both climatic warming and fluctuations.},  Author = {Campos, Paula F. and Willerslev, Eske and Sher, Andrei and Orlando, Ludovic and Axelsson, Erik and Tikhonov, Alexei and Aaris-S{\o}rensen, Kim and Greenwood, Alex D. and Kahlke, Ralf-Dietrich and Kosintsev, Pavel and Krakhmalnaya, Tatiana and Kuznetsova, Tatyana and Lemey, Philippe and MacPhee, Ross and Norris, Christopher A. and Shepherd, Kieran and Suchard, Marc A. and Zazula, Grant D. and Shapiro, Beth and Gilbert, M. Thomas P.},  Doi = {10.1073/pnas.0907189107},  Eprint = {http://www.pnas.org/content/107/12/5675.full.pdf+html},  Journal = {Proceedings of the National Academy of Sciences},  Number = {12},  Pages = {5675-5680},  Title = {Ancient DNA analyses exclude humans as the driving force behind late Pleistocene musk ox (Ovibos moschatus) population dynamics},  Volume = {107},  Year = {2010},  Bdsk-Url-1 = {http://dx.doi.org/10.1073/pnas.0907189107}}  @article{Faria2012453,  Author = {Faria, Nuno R. and Suchard, Marc A. and Abecasis, Ana and Sousa, Jo{\~a}o D. and Ndembi, Nicaise and Bonfim, Idalina and Camacho, Ricardo J. and Vandamme, Anne-Mieke and Lemey, Philippe},  Doi = {10.1016/j.meegid.2011.04.028},  Issn = {1567-1348},  Journal = {Infection, Genetics and Evolution},  Keywords = {Cameroon},  Number = {2},  Pages = {453 - 460},  Title = {Phylodynamics of the HIV-1 CRF02\_AG clade in Cameroon},  Volume = {12},  Year = {2012},  Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.meegid.2011.04.028}}  @article{monjane2011reconstructing,  Author = {Monjane, Ad{\'e}rito L and Harkins, Gordon W and Martin, Darren P and Lemey, Philippe and Lefeuvre, Pierre and Shepherd, Dionne N and Oluwafemi, Sunday and Simuyandi, Michelo and Zinga, Innocent and Komba, Ephrem K and others},  Journal = {Journal of virology},  Number = {18},  Pages = {9623--9636},  Publisher = {Am Soc Microbiol},  Title = {Reconstructing the history of Maize streak virus strain A dispersal to reveal diversification hot spots and its origin in southern Africa},  Volume = {85},  Year = {2011}}  @article{vijaykrishna2011long,  Author = {Vijaykrishna, Dhanasekaran and Smith, Gavin JD and Pybus, Oliver G and Zhu, Huachen and Bhatt, Samir and Poon, Leo LM and Riley, Steven and Bahl, Justin and Ma, Siu K and Cheung, Chung L and others},  Journal = {Nature},  Number = {7348},  Pages = {519--522},  Publisher = {Nature Publishing Group},  Title = {Long-term evolution and transmission dynamics of swine influenza A virus},  Volume = {473},  Year = {2011}}  @article{mutreja2011evidence,  Author = {Mutreja, Ankur and Kim, Dong Wook and Thomson, Nicholas R and Connor, Thomas R and Lee, Je Hee and Kariuki, Samuel and Croucher, Nicholas J and Choi, Seon Young and Harris, Simon R and Lebens, Michael and others},  Journal = {Nature},  Number = {7365},  Pages = {462--465},  Publisher = {Nature Publishing Group},  Title = {Evidence for several waves of global transmission in the seventh cholera pandemic},  Volume = {477},  Year = {2011}}  @article{pybus2012unifying,  Author = {Pybus, O. G. and Suchard, M. A. and Lemey, P. and Bernardin, F. J. and Rambaut, A. and Crawford, F. W. and Gray, R. R. and Arinaminpathy, N. and Stramer, S. L. and Busch, M. P. and others},  Date-Modified = {2014-07-06 02:07:13 +0000},  Journal = {Proceedings of the National Academy of Sciences},  Number = {37},  Pages = {15066--15071},  Publisher = {National Acad Sciences},  Title = {Unifying the spatial epidemiology and molecular evolution of emerging epidemics},  Volume = {109},  Year = {2012}}  @article{leache2011accuracy,  Author = {Leach{\'e}, Adam D and Rannala, Bruce},  Journal = {Systematic Biology},  Number = {2},  Pages = {126--137},  Publisher = {Oxford University Press},  Title = {The accuracy of species tree estimation under simulation: a comparison of methods},  Volume = {60},  Year = {2011}}  @article{liu2008best,  Author = {Liu, Liang},  Journal = {Bioinformatics},  Number = {21},  Pages = {2542--2543},  Publisher = {Oxford Univ Press},  Title = {BEST: Bayesian estimation of species trees under the coalescent model},  Volume = {24},  Year = {2008}}  @article{wong2008alignment,  Author = {Wong, K. M. and Suchard, M. A. and Huelsenbeck, J. 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