Data from: Cell tropism predicts long-term nucleotide substitution rates of mammalian RNA viruses

The high rates of RNA virus evolution are generally attributed to
replication with error-prone RNA-dependent RNA polymerases. However, these
long-term nucleotide substitution rates span three orders of magnitude and
do not correlate well with mutation rates or selection pressures. This
substitution rate variation may be explained by differences in virus
ecology or intrinsic genomic properties. We generated nucleotide
substitution rate estimates for mammalian RNA viruses and compiled
comparable published rates, yielding a dataset of 118 substitution rates
of structural genes from 51 different species, as well as 40 rates of
non-structural genes from 28 species. Through ANCOVA analyses, we
evaluated the relationships between these rates and four ecological
factors: target cell, transmission route, host range, infection duration;
and three genomic properties: genome length, genome sense, genome
segmentation. Of these seven factors, we found target cells to be the only
significant predictors of viral substitution rates, with tropisms for
epithelial cells or neurons (P<0.0001) as the most significant
predictors. Further, one-tailed t-tests showed that viruses primarily
infecting epithelial cells evolve significantly faster than neurotropic
viruses (P<0.0001 and P<0.001 for the structural genes and
non-structural genes, respectively). These results provide strong evidence
that the fastest evolving mammalian RNA viruses infect cells with the
highest turnover rates: the highly proliferative epithelial cells.
Estimated viral generation times suggest that epithelial-infecting viruses
replicate more quickly than viruses with different cell tropisms. Our
results indicate that cell tropism is a key factor in viral evolvability.