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ABSTRACT
Coinfection in RNA virus populations results in two important phenomena, complementation and recombination. Of the two, complementation has a strong effect on selection against deleterious mutations, as has been confirmed in earlier studies. As complementation delays the purging of less-fit mutations, coinfection may be detrimental to the evolution of a virus population. Here we employ both deterministic modeling and stochastic simulation to explore the mechanisms underlying the interactions between complementation and other evolutionary factors, namely, mutation, selection, and epistasis. We find that strong complementation reduces slightly the overall fitness of a virus population but substantially enhances its diversity and robustness, especially when interacting with selection and epistasis.
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RNA viruses infect many organisms. They have high mutation rates, compact segmented genomes, very short generation times, huge population sizes, and substantial diversity within populations (Chao 1988; Wilke and Novella 2003; Froissart et al. 2004; Elena et al. 2006). These properties enable RNA viruses to change continuously and adapt easily to adverse environments, posing continual challenges for antiviral therapies and vaccinations. Current research on RNA viruses has turned to theoretical population genetics and evolutionary theory for novel and practical approaches for management of viral diseases (e.g., Turner and Chao 1999, 2003; Burch et al. 2003; Burch and Chao 2004; Dennehy and Turner 2004; Moya et al. 2004; Bretscher et al. 2004; Sanjua?n et al. 2005; Boni et al. 2006).
Coinfection, where multiple viruses infect a cell simultaneously, is important in the life cycle of RNA viruses. During coinfection, haploid viral genomes act in a manner similar to those of diploid organisms, exchanging genetic material randomly or preferentially. Reassortment of genomesegmentsmay create severely deleterious mutational combinations, thus speeding up the elimination of mutational load. Coinfection may, however, result in complementation, where viruses carrying different deleterious mutations may benefit from the normal products that each can produce, so that both types of viruses can be represented in the offspring. In contrast to recombination, complementation weakens the selection against deleteriousmutations. In this way, it contributes to the stability of the whole virus population as itmaintains a high level of diversity without sacrificing the overall fitness of the population.
Froissart et al. (2004) investigated whether complementation or random reassortment would have the stronger effect on...