Abstract
BackgroundEvolutionary theory suggests that the selection pressure on parasites to maximize their transmission determines their optimal host exploitation strategies and thus their virulence. Establishing the adaptive basis to parasite life history traits has important consequences for predicting parasite responses to public health interventions. In this study we examine the extent to which malaria parasites conform to the predicted adaptive trade-off between transmission and virulence, as defined by mortality. The majority of natural infections, however, result in sub-lethal virulent effects (e.g. anaemia) and are often composed of many strains. Both sub-lethal effects and pathogen population structure have been theoretically shown to have important consequences for virulence evolution. Thus, we additionally examine the relationship between anaemia and transmission in single and mixed clone infections.ResultsWhereas there was a trade-off between transmission success and virulence as defined by host mortality, contradictory clone-specific patterns occurred when defining virulence by anaemia. A negative relationship between anaemia and transmission success was found for one of the parasite clones, whereas there was no relationship for the other. Notably the two parasite clones also differed in a transmission phenotype (gametocyte sex ratio) that has previously been shown to respond adaptively to a changing blood environment. In addition, as predicted by evolutionary theory, mixed infections resulted in increased anaemia. The increased anaemia was, however, not correlated with any discernable parasite trait (e.g. parasite density) or with increased transmission.ConclusionsWe found some evidence supporting the hypothesis that there is an adaptive basis correlating virulence (as defined by host mortality) and transmission success in malaria parasites. This confirms the validity of applying evolutionary virulence theory to biomedical research and adds support to the prediction that partially effective vaccines may select for increasingly virulent malaria parasite strains. By contrast, there was no consistent correlation between transmission and sub-lethal anaemia, a more common outcome of malaria infection. However, overall, the data are not inconsistent with the recent proposal that sub-lethal effects may impose an upper limit on virulence. Moreover, clone specific differences in transmission phenotypes linked to anaemia do suggest that there is considerable adaptive potential relating anaemia and transmission that may lead to uncertain consequences following intervention strategies.
Highlights
Evolutionary theory suggests that the selection pressure on parasites to maximize their transmission determines their optimal host exploitation strategies and their virulence
We first considered infection by injection of 106 infected red blood cells of either of two clones of P. gallinaceum or an equal mix of the two
We found (i) that in both infected red blood cells (iRBC) and sporozoite-induced infections, transmission success was positively correlated with host mortality rate but (ii) that there was a total transmission cost to host death only if the host died before the completion of the transmission period; if the host died after completing the acute transmission period there was no impact on total transmission
Summary
Evolutionary theory suggests that the selection pressure on parasites to maximize their transmission determines their optimal host exploitation strategies and their virulence. Pathogens are expected to evolve a schedule of host exploitation that maximises their transmission and there are an increasing number of experimental studies demonstrating a relationship between transmission and virulence [5,6,7,8] Incorporation of such virulence theory into an epidemiological framework has led to the suggestion that partially effective vaccines targeting pathogen virulence traits (e.g. malaria parasite growth rate) may lead to the selection of increased pathogen virulence [9]. Identifying the biological determinants governing the constraint between the transmission/virulence trade-off in turn requires an appreciation of the host-pathogen system in question This has been recently exemplified by the case of the bacteria Neisseria meningitides, where virulence arises through colonisation of atypical tissues with no apparent direct benefit for transmission [11]. There is an indirect trade-off between virulence and transmission that is strongly influenced by the time lag occurring between the beneficial and deleterious outcomes of within-host evolution [13]
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