Why do RNA viruses recombine?

Abstract

Recombination occurs in many RNA viruses and can be of major evolutionary significance. However, rates of recombination vary dramatically among RNA viruses, which can range from clonal to highly recombinogenic. Here, we review the factors that might explain this variation in recombination frequency and show that there is little evidence that recombination is favoured by natural selection to create advantageous genotypes or purge deleterious mutations, as predicted if recombination functions as a form of sexual reproduction. Rather, recombination rates seemingly reflect larger-scale patterns of viral genome organization, such that recombination may be a mechanistic by-product of the evolutionary pressures acting on other aspects of virus biology.

Virological factors that increase the transmissibility of emerging human viruses

“…Recombination rates vary extensively among RNA viruses, from seemingly clonal in nonsegmented negative-sense RNA viruses (i.e., the order Mononegavirales) to per site rates that are greater than that of mutation in the case of HIV-1 and that undoubtedly have a major impact on their evolution and epidemiology (39). Although recombination has the potential to facilitate transmissibility by accelerating the rate at which advantageous genetic combinations are produced compared with mutation alone, frequent recombination will also break up beneficial genetic configurations, and clonal viruses like those species of the Mononegavirales are readily able to emerge in new hosts (for example, Ebola virus) (50). Indeed, there are few cases in which recombination has been shown to underpin successful cross-species transmission and emergence (39).…”

Diversity of Plant Virus Populations: A Valuable Tool for Epidemiological Studies

“…It may take place through recombination, when the switched information consists on segments of nucleotide strands of different genetic variants, or through reassortment of whole genomic segments in viruses with segmented genomes, a process which is also known as pseudorecombination [9].…”

“…For instance, a population may become extinct because of an excessive accumulation of mutations, a phenomenon known as lethal mutagenesis [36], which also takes place in viruses and is an interesting mechanism for antiviral therapies [37]. Also, high mutation rates combined to small sizes of asexual populations (as a result of genetic bottlenecks, see below) may led to the progressive accumulation of deleterious mutations and the loss of mutation-free individuals, with a consequent reduction in fitness in populations, which is called the "Muller's ratchet" [9,38]. In addition to the adaptive relevance of genetic exchange to create beneficial genomic combinations, recombination and reassortment may represent a sexual mechanism contributing to compensate the accumulation of deleterious mutations and the effect of "Muller's ratchet" in populations, and it has been postulated as a theory of evolution of sex in RNA viruses [9,39].…”

The emergence of drug resistant HIV variants and novel anti–retroviral therapy

“…The retroviral infection is characterized by numerous shifts and diversification of nucleotides during replication [12,13] . As an infidel reverse transcriptase (RT), the rate of nucleotide shifts occurring during replication of HIV is six orders of magnitude more than the replication of a mammalian genome, allocating to a heterogeneous crowd of virions within host bodily systems [14] . Such prominent inaccuracy of retroviral RT results from a lack of proofreading in combination with a physically large active site [15] .…”