The classical view of sex ratio evolution, popularized by R. A. Fisher, is that the sex ratio at birth should be equal when males and females require the same level of parental investment. Thus, although differences in mortality between the sexes during parental investment will cause deviations from an equal sex ratio at birth, differential mortality after parental investment should have no effect. However, a recent theoretical model appears to contradict this view, suggesting that differential mortality after the period of parental investment does cause deviations from an equal sex ratio at birth. Moreover, the life stage at which mortality differs (juvenile vs. adult) is predicted to cause contrasting effects on sex ratio evolution. These results are in stark contrast with Fisher's hypothesis. Here, we resolve this disparity by analyzing a stage-and sex-structured model of population dynamics. We find that selection always drives the population to an equal sex ratio at birth regardless of differential mortality effects after parental investment, thus confirming Fisher's hypothesis. The disparity appears to be due to incorrect accounting of mutant-resident unions, which we avoid by considering separate union classes for different types of mutant-resident unions.

No abstract

No abstract

AbstractThe epidemiology of sexually transmitted infections (STIs) is inherently linked to host mating dynamics. Studies across many taxa show that adult sex ratio, a major determinant of host mating dynamics, is often skewed – sometimes strongly – toward males or females. However, few predictions exist for the effects of skewed sex ratio on STI epidemiology, and none when coupled with sex biased disease characteristics. Here we use mathematical modelling to examine how interactions between sex ratio and disease characteristics affect STI prevalence in males and females. Notably, we find that while overall disease prevalence peaks at equal sex ratios, prevalence per sex peaks at skewed sex ratios. Furthermore, disease characteristics, sex-biased or not, drive predictable differences in male and female STI prevalence as sex ratio varies, with higher transmission and lower virulence generally increasing differences between the sexes for a given sex ratio. These findings may be due to a balance between increased per-capita mating in the less common sex, and a reduction in mating rate – hence disease prevalence – at the population level. Our work reveals new insights into how STI prevalence in males and females depends on a complex interaction between host population demography and disease characteristics.