Mutation and recombination are central processes driving microbial evolution. A high mutation rate fuels adaptation but also generates deleterious mutations. Recombination between two different genomes may resolve this paradox, alleviating effects of clonal interference and purging deleterious mutations. Here we demonstrate that recombination significantly accelerates adaptation and evolution during acute virus infection. We identified a poliovirus recombination determinant within the virus polymerase, mutation of which reduces recombination rates without altering replication fidelity. By generating a panel of variants with distinct mutation rates and recombination ability, we demonstrate that recombination is essential to enrich the population in beneficial mutations and purge it from deleterious mutations. The concerted activities of mutation and recombination are key to virus spread and virulence in infected animals. These findings inform a mathematical model to demonstrate that poliovirus adapts most rapidly at an optimal mutation rate determined by the trade-off between selection and accumulation of detrimental mutations.
Bibliographical noteFunding Information:
We thank Drs. Judith Frydman, Colin Parish, Edward C. Holmes, Jeremy Draghi, and members of the Andino lab for critical comments. This work was supported by NIH ( R01, AI36178 , AI40085 , P01 AI091575 ) and the University of California (CCADD) and by DoD-DARPA Prophecy. We thank Rebecca Batorsky for sharing her Monte Carlo code for viral evolution. I.M.R. thanks Irvin “Tack” Kuntz for his hospitality and financial support.
© 2016 Elsevier Inc.
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