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Virulence evolution in a host-parasite system in the absence of viral evolution.

ABSTRACT: QUESTION:How does virulence evolve in the Drosophila melanogaster/sigma virus (DMelSV) system? ORGANISMS:Drosophila melanogaster (host) and DMelSV (parasite). EMPIRICAL METHODS:Artificial selection on whole-carcass viral titre of infected flies, including two selection regimes (maternal and biparental transmission) and three treatments within each regime (increased titre, decreased titre, and control). The maternal transmission selection regime lasted for six generations, while the biparental transmission selection regime lasted for twelve generations. We further quantified virulence by estimating the fecundity, viability, and development time of infected flies. Finally, we sequenced virus strains at the end of selection. PREDICTIONS AND CONCLUSIONS:Titre is defined here as the number of viral genomes inside a single fly, while virulence is defined as harm to host. We predicted that titre would respond to both increased and decreased selection, that virulence would evolve as a positively correlated response, and that sequence evolution in the viruses would be responsible for these changes. Titre did respond to selection in the biparental regime, although both high and control lines both demonstrated increased titre, while the titre of the low lines did not change. One component of virulence, development time, was positively correlated with titre in the biparental transmission lines (maternal transmission lines were not scored for virulence). However, we detected few (and in some cases, no) genomic changes in the virus, making viral evolution unlikely to be responsible for the response to selection and the association between development time and titre.

SUBMITTER: Brusini J

PROVIDER: S-EPMC5315458 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Virulence evolution in a host-parasite system in the absence of viral evolution.

Brusini J J Wang Y Y Matos L F LF Sylvestre L-S LS Bolker B M BM Wayne M L ML

Evolutionary ecology research 20130101

<h4>Question</h4>How does virulence evolve in the <i>Drosophila melanogaster</i>/sigma virus (DMelSV) system?<h4>Organisms</h4><i>Drosophila melanogaster</i> (host) and DMelSV (parasite).<h4>Empirical methods</h4>Artificial selection on whole-carcass viral titre of infected flies, including two selection regimes (maternal and biparental transmission) and three treatments within each regime (increased titre, decreased titre, and control). The maternal transmission selection regime lasted for six ...[more]

PMID: 28217033

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Project description:Virulence, the degree to which a pathogen harms its host, is an important but poorly understood aspect of host-pathogen interactions. Virulence is not static, instead depending on ecological context and potentially evolving rapidly. For instance, at the start of an epidemic, when susceptible hosts are plentiful, pathogens may evolve increased virulence if this maximizes their intrinsic growth rate. However, if host density declines during an epidemic, theory predicts evolution of reduced virulence. Although well-studied theoretically, there is still little empirical evidence for virulence evolution in epidemics, especially in natural settings with native host and pathogen species. Here, we used a combination of field observations and lab assays in the Daphnia-Pasteuria model system to look for evidence of virulence evolution in nature. We monitored a large, naturally occurring outbreak of Pasteuria ramosa in Daphnia dentifera, where infection prevalence peaked at ~ 40% of the population infected and host density declined precipitously during the outbreak. In controlled infections in the lab, lifespan and reproduction of infected hosts was lower than that of unexposed control hosts and of hosts that were exposed but not infected. We did not detect any significant changes in host resistance or parasite infectivity, nor did we find evidence for shifts in parasite virulence (quantified by host lifespan and number of clutches produced by hosts). However, over the epidemic, the parasite evolved to produce significantly fewer spores in infected hosts. While this finding was unexpected, it might reflect previously quantified tradeoffs: parasites in high mortality (e.g., high predation) environments shift from vegetative growth to spore production sooner in infections, reducing spore yield. Future studies that track evolution of parasite spore yield in more populations, and that link those changes with genetic changes and with predation rates, will yield better insight into the drivers of parasite evolution in the wild.Supplementary informationThe online version contains supplementary material available at 10.1007/s10682-022-10169-6.

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Virulence evolution in a host-parasite system in the absence of viral evolution.

Publications

Virulence evolution in a host-parasite system in the absence of viral evolution.

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