Feline panleukopenia (FPL) is a severe, often fatal disease caused by feline parvovirus (FPV). How infection with FPV might impact the composition of the entire eukaryotic enteric virome in cats has not been characterized. We used metatranscriptomic and viral particle enrichment metagenomic approaches to characterize the enteric viromes of 23 cats naturally infected with FPV (FPV-cases) and 36 age-matched healthy shelter cats (healthy controls). Sequencing reads were detected from 11 mammalian infecting viral families mostly belonging to Coronaviridae, Parvoviridae and Astroviridae. Among the healthy control cats the most abundant viruses were Feline coronavirus, Mamastrovirus 2 and Carnivore bocaparvovirus 3 (Feline bocavirus 1) with frequent co-infections of all three. Feline chaphamaparvovirus was only detected in healthy controls (6/36, 16.7%). Among the FPV-cases, in addition to FPV, the most abundant viruses were Mamastrovirus 2, Feline coronavirus and Carnivore bocaparvovirus 4 (Feline bocaparvovirus 2). The latter and Feline bocaparvovirus 3 were detected significantly more frequently in FPV-cases than in healthy controls. Feline calicivirus was present in a high proportion of FPV-cases (11/23, 47.8%) compared to healthy controls (5/36, 13.9%, p=0.0067). Feline kobuvirus infections were also common among FPV-cases (9/23, 39.1%) and were not detected in any healthy control cats (p<0.0001). While abundant in both groups, astroviruses were more frequently present in FPV-cases (19/23, 82.6%) than in healthy controls (18/36, p=0.0142). The differences in eukaryotic virome composition found in this study indicate that further investigations to determine associations between enteric viral co-infections on clinical disease severity in cats with FPL are warranted.

SUMMARY The 2013-2015 Ebola virus disease (EVD) epidemic is caused by the Makona variant of Ebola virus (EBOV). Early in the epidemic, genome sequencing provided insights into virus evolution and transmission, and offered important information for outbreak response. Here we analyze sequences from 232 patients sampled over 7 months in Sierra Leone, along with 86 previously released genomes from earlier in the epidemic. We confirm sustained human-to-human transmission within Sierra Leone and find no evidence for import or export of EBOV across national borders after its initial introduction. Using high-depth replicate sequencing, we observe both host-to-host transmission and recurrent emergence of intrahost genetic variants. We trace the increasing impact of purifying selection in suppressing the accumulation of nonsynonymous mutations over time. Finally, we note changes in the mucin-like domain of EBOV glycoprotein that merit further investigation. These findings clarify the movement of EBOV within the region and describe viral evolution during prolonged human-to-human transmission.