High Frequency of Mutations That Expand the Host Range of an RNA Virus

Abstract

The ability of a virus population to colonize a novel host is predicted to depend on the equilibrium frequency of potential colonists (i.e., genotypes capable of infecting the novel host) in the source population. In this study, we investigated the determinants of the equilibrium frequency of potential colonists in the RNA bacteriophage f6. We isolated 40 spontaneous mutants capable of infecting a novel Pseudomonas syringae host and sequenced their host attachment genes to identify the responsible mutations. We observed 16 different mutations in the host attachment gene and used a new statistical approach to estimate that 39 additional mutations were missed by our screen. Phenotypic and fitness assays confirmed that the proximate mechanism underlying host range expansion was an increase in the ability to attach to the novel host and that acquisition of this ability most often imposed a cost for growth rate on two standard hosts. Considered in a population genetic framework, our data suggest that host range mutations should exist in phage populations at an equilibrium frequency (3 3 10 À4) that exceeds the phage mutation rate by more than two orders of magnitude. Thus, colonization of novel hosts is unlikely to be limited by an inability to produce appropriate mutations.

Understanding the limits to generalizability of experimental evolutionary models

“…We also incorporate two well-established trade-offs: increasing the range of resistance to phage leads to a decrease in growth rate [14][15][16] and increase in the number of hosts a phage can infect comes at a reproductive cost through a combination of trade-offs with adsorption rate and burst size 14,17 .…”

New enveloped dsRNA phage from freshwater habitat

“…Such a phenomenon could also explain the higher sequence variability between the M-segments of wNN and w6 compared with the other two segments. Furthermore, strong selection pressure is presumably exerted on the M-segmentencoded proteins during co-evolution with the host, as demonstrated by the susceptibility of the host attachment protein P3 of w6 to spontaneous mutations, resulting in phages with varying host range (Duffy et al, 2006;Ferris et al, 2007). Recombination by crossing-over with genetic material of the host cell or other viruses is an unlikely explanation for the observed sequence variation (Onodera et al, 2001) as homologous sequences for wNN were not found outside previously identified cystoviruses.…”

“…The genetic plasticity allows RNA viruses to rapidly adapt to challenges posed by the environment, manifested e.g. by evasion of host immune response (Malim & Emerman, 2001), evolution of resistance to antiviral drugs (Nora et al, 2007), increase in virulence (Khatchikian et al, 1989) or host-range expansion (Brown, 1997;Duffy et al, 2006;Ferris et al, 2007;Gibbs & Weiller, 1999).…”

“…Surprisingly, the rate of reassortment may vary among populations sampled from different geographical locations (O'Keefe et al, 2010). Additional genetic diversity is acquired via mutations occurring at the rate of y10 26 per locus per generation Chao et al, 2002;Ferris et al, 2007), although higher values have also been suggested, especially in terms of host-range mutations (Ferris et al, 2007).…”

Resposta de genótipos de citros à leprose e variabilidade genética da ORF p29 do vírus da leprose dos citros C (CiLV-C)

“…Entretanto, algumas dessas mudanças, que são deletérias no hospedeiro atual, podem ser adaptativas sob diferentes condições (DUFFY et al, 2006;FERRIS et al, 2007), como em outros hospedeiros. A taxa de variabilidade genética depende da espécie de hospedeiro infectada, embora os mecanismos responsáveis por essa taxa de variação sejam desconhecidos (PITA et al, 2007) (SPEGAZZINI, 1920;BITTANCOURT, 1955;VERGANI, 1945), tendo ficado restrita a Paraguai, Argentina e Brasil por cerca de 80 anos (BASTIANEL et al, 2010).…”