Abstract

Many insect species are infected with maternally transmitted endosymbionts, the most widely documented being Wolbachia. The rate of spread and equilibrium of prevalence of these infections depend on two parameters – maternal transmission fidelity and relative fitness of infected cytoplasmic lineages. Both transmission fidelity and the phenotypic effect of endosymbionts often increase with endosymbiont density within hosts. Thus, the dynamics of infection prevalence in host populations depends on processes affecting within‐host density of endosymbionts. In theory, the equilibrium prevalence of infection by male‐killing endosymbionts is much more sensitive to changes in transmission fidelity and relative fitness than is that of endosymbionts that cause cytoplasmic incompatibility. In natural populations, male‐killers exhibit much greater temporal and spatial variation in the prevalence of infection than do endosymbionts that cause cytoplasmic incompatibility. Thus, the population dynamics of endosymbiont infections, especially those that cause male‐killing, is likely to be governed by environmental and genetic variables that affect within‐host density of these infections.

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