Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Apr 27;13(4):e1006254.
doi: 10.1371/journal.ppat.1006254. eCollection 2017 Apr.

The not-so-infinite malleability of RNA viruses: Viral and cellular determinants of RNA virus mutation rates

Affiliations
Review

The not-so-infinite malleability of RNA viruses: Viral and cellular determinants of RNA virus mutation rates

Everett Clinton Smith. PLoS Pathog. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

The author has declared that no competing interests exist.

Figures

Fig 1
Fig 1. Large viral population sizes buffer against deleterious and lethal mutations.
Mutations generated via virus- and cell-dependent mechanisms can differentially impact viral fitness. Viruses are depicted as colored spheres corresponding to the presence of beneficial, neutral, deleterious, or lethal mutations. Population size is depicted by the diagonal arrow and increasing square size. High mutation rates result in a phenotypically diverse viral population (“mutation rate” panel), but the frequency at which these variants appear in a population (“mutation frequency” panel) depends upon genetic drift and natural selection. As such, large population sizes are critical for buffering the viral population against the effects of deleterious and lethal mutations. The ratios of beneficial, neutral, deleterious, and lethal mutations are based on data from vesicular stomatitis virus (VSV) [1].

References

    1. Sanjuán R, Moya A, Elena SF. The distribution of fitness effects caused by single-nucleotide substitutions in an RNA virus. Proc Natl Acad Sci U S A. 2004;101: 8396–8401. 10.1073/pnas.0400146101 - DOI - PMC - PubMed
    1. Visher E, Whitefield SE, McCrone JT, Fitzsimmons W, Lauring AS. The mutational robustness of Influenza A virus. PLoS Pathog. 2016;12: e1005856 10.1371/journal.ppat.1005856 - DOI - PMC - PubMed
    1. Sanjuán R, Nebot MR, Chirico N, Mansky LM, Belshaw R. Viral mutation rates. J Virol. 2010;84: 9733–9748. 10.1128/JVI.00694-10 - DOI - PMC - PubMed
    1. Steinhauer DA, Domingo E, Holland JJ. Lack of evidence for proofreading mechanisms associated with an RNA virus polymerase. Gene. 1992;122: 281–288. - PubMed
    1. Sale JE, Lehmann AR, Woodgate R. Y-family DNA polymerases and their role in tolerance of cellular DNA damage. Nat Rev Mol Cell Biol. 2012;13: 141–152. 10.1038/nrm3289 - DOI - PMC - PubMed

Publication types

LinkOut - more resources