Sexual selection in mammals has resulted in the evolution of sexual size dimorphism (SSD), with males usually being the larger sex. Comparative analyses indicate that the evolution of SSD is associated with the evolution of male-biased mortality, suggesting a possible causal link between the two. Here, we use a comparative approach to investigate the possible role of parasites in generating this relation. We show that there is a robust association between male-biased parasitism and the degree of sexual selection, as measured by mating system (monogamous or polygynous) and by the degree of SSD. There is also a positive correlation, across taxa, between male-biased mortality and male-biased parasitism. These results are consistent with the hypothesis that parasites contribute to the observed association between SSD and male-biased mortality.

Antagonistic coevolution between hosts and parasites has been proposed as a mechanism maintaining genetic diversity in both host and parasite populations. In particular, the high levels of genetic diversity widely observed at the major histocompatibility complex (MHC) of vertebrate hosts are consistent with the hypothesis of parasite-driven balancing selection acting to maintain MHC genetic diversity. To date, however, empirical evidence in support of this hypothesis, especially from natural populations, has been lacking. A large unmanaged population of Soay sheep (Ovis aries L.) is used to investigate associations between MHC variation, juvenile survival, and parasite resistance. We show in an unmanaged, nonhuman population that allelic variation within the MHC is significantly associated with differences in both juvenile survival and resistance to intestinal nematodes. Certain MHC alleles are associated with low survivorship probabilities and high levels of parasitism or vice versa. We conclude that parasites are likely to play a major role in the maintenance of MHC diversity in this population.

Mounting effective resistance against pathogens is costly in terms of energy and nutrients. However, it remains unexplored whether hosts can offset such costs by adjusting their dietary intake so as to recoup the specific resources involved. We test this possibility by experimentally challenging caterpillars (Spodoptera littoralis) with a highly virulent entomopathogen (nucleopolyhedrovirus), under dietary regimes varying in the content of protein and digestible carbohydrate. We found that dietary protein influenced both resistance to pathogen attack and constitutive immune function to a greater extent than did dietary carbohydrate, indicating higher protein costs of resistance than energy costs. Moreover, when allowed to self-compose their diet, insects surviving viral challenge increased their relative intake of protein compared with controls and those larvae dying of infection, thus demonstrating compensation for protein costs associated with resistance. These results suggest that the change in the host's nutritional demands to fight infection induces a compensatory shift in feeding behaviour.