Abstract
BackgroundTrade-offs between anti-parasite defence mechanisms and other life history traits limit the evolution of host resistance to parasites and have important implications for understanding diseases such as malaria. Mosquitoes have not evolved complete resistance to malaria parasites and one hypothesis is that anti-malaria defence mechanisms are costly.ResultsWe used matrix population models to compare the population growth rates among lines of Anopheles gambiae that had been selected for resistance or high susceptibility to the rodent malaria parasite, Plasmodium yoelii nigeriensis. The population growth rate of the resistant line was significantly lower than that of the highly susceptible and the unselected control lines, regardless of whether mosquitoes were infected with Plasmodium or not. The lower population growth of malaria-resistant mosquitoes was caused by reduced post blood-feeding survival of females and poor egg hatching.ConclusionWith respect to eradicating malaria, the strategy of releasing Plasmodium-resistant Anopheles mosquitoes is unlikely to be successful if the costs of Plasmodium-resistance in the field are as great as the ones measured in this study. High densities of malaria-resistant mosquitoes would have to be maintained by continuous release from captive breeding facilities.
Highlights
Trade-offs between anti-parasite defence mechanisms and other life history traits limit the evolution of host resistance to parasites and have important implications for understanding diseases such as malaria
We found that the malaria-resistant A. gambiae mosquitoes have a lower population growth rate than malaria-susceptible mosquitoes
The population growth rate of the refractory genotype was always lower than that of the highly susceptible genotype (Figure 1). This suggests that the immune mechanisms required for complete refractoriness to P. yoelii nigeriensis are costly for A. gambiae and would not evolve under the laboratory conditions used in this study
Summary
Trade-offs between anti-parasite defence mechanisms and other life history traits limit the evolution of host resistance to parasites and have important implications for understanding diseases such as malaria. Theory predicts that the evolution of these resistance mechanisms in the host is constrained by antagonistic pleiotropy, when one allele affects two or more traits with opposite effects on fitness [2,3]. Such costs of evolving resistance have been demonstrated by measuring negative genetic correlations (genetic trade-offs) between immunity and other life history traits in selection or quantitative genetic experiments [4,5,6,7,8,9]. This is important because the evolution of (page number not for citation purposes)
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