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...
\begin{table}
\begin{tabular}{ c c | c | p{3cm}p{8cm}}
\hline
Seg&Replicate (E)&$d_0$&Signal
$S_3^{d_0}$&Noise $S_3^{d_0}replace_contentNoise $S_2^{d_0}$\\
\hline
1 & 1 & 8.713 & $\emptyset$ & 33, 281, 404, 824, 839, 926, 1889, 2290, 2298, \textcolor{blue}{2299}, \textcolor{blue}{2303}\\
& 2 & 9.138 & 2072 & 311, \textcolor{blue}{2299}, \textcolor{blue}{2303}\\
...
Taking the intersection of the findings from both replicates, we identify only S6-822 as a substitution site due to the treatment, along with S1-2299, S2-2303, S3-173, S3-174, S3-176, S3-176, S3-200, S3-203, S3-2078, S3-2192, S3-2193, S3-2195, S5-24, S5-389, S5-1103, S6-977 as the locations with large variation not due to the treatment.
Comparing the result in Foll et
all al \citep{Foll2014} to our findings (Table \ref{tab:H1N14t}), we notice that all the extra locations identified there appear in the result for the first biological replicate, but not in the result for the second. This phenomena is likely caused by the fact that the average read count per site for the second replicate is much
less smaller than the first. The
analysis in Foll \citep{Foll2014} based on a population genetic
base approach
is therefore
biased appears to be heavily influenced by the first replicate.
It This leads us to postulate that their result is adversely affected by the large imbalance in counts.
With addition samples, we Noticing that the two additional sites identified in Table \ref{tab:H1N15t} show more pronounced drug effect after the 12th passage (see Figures \ref{fig:S5-300},\ref{fig:S8-80}). We conclude that IVA had not fully responded to the treatment by Passage 12 and our previous analysis, including the last time point collection, is more reliable for the identification of substitution sites.