Males and females vary in many characteristics that typically underlie how well a host is able to fight infection, such as body-size, immune capacity, or energy availability. Although well studied in the context of sexual signalling, there is now growing recognition that these differences can influence aspects of pathogen evolution as well. Here we consider how co-infection between multiple pathogen strains is shaped by male-female differences. In natural populations, infections by more than one pathogen strain or species are believed to be a widespread occurrence. Using the water flea, Daphnia magna, we exposed genetically identical males and females to replicated bacterial co-infections. We found that pathogen transmission and virulence were much higher in females. However, males did not simply lower average pathogen fitness, but rather the influence of co-infection was more varied and less defined than in females. We discuss how pathogens may have more fitness benefits to gain, and consequently to lose, when infecting one sex over the other.
The patterns of immunity conferred by host sex or age represent two sources of host heterogeneity that can potentially shape the evolutionary trajectory of disease. With each host sex or age encountered, a pathogen's optimal exploitative strategy may change, leading to considerable variation in expression of pathogen transmission and virulence. To date, these host characteristics have been studied in the context of host fitness alone, overlooking the effects of host sex and age on the fundamental virulence-transmission trade-off faced by pathogens. Here, we explicitly address the interaction of these characteristics and find that host sex and age at exposure to a pathogen affect age-specific patterns of mortality and the balance between pathogen transmission and virulence. When infecting age-structured male and female Daphnia magna with different genotypes of Pasteuria ramosa, we found that infection increased mortality rates across all age classes for females, whereas mortality only increased in the earliest age class for males. Female hosts allowed a variety of trade-offs between transmission and virulence to arise with each age and pathogen genotype. In contrast, this variation was dampened in males, with pathogens exhibiting declines in both virulence and transmission with increasing host age. Our results suggest that differences in exploitation potential of males and females to a pathogen can interact with host age to allow different virulence strategies to coexist, and illustrate the potential for these widespread sources of host heterogeneity to direct the evolution of disease in natural populations.
Sex and infection are intimately linked. Many diseases are spread by sexual contact, males are thought to evolve exaggerated sexual signals to demonstrate their immune robustness, and pathogens have been shown to direct the evolution of recombination. In all of these examples, infection is influencing the evolution of male and female fitness, but less is known about how sex differences influence pathogen fitness. A defining characteristic of sexual dimorphism is not only divergent phenotypes, but also a complex genetic architecture involving changes in genetic correlations among shared fitness traits, and differences in the accumulation of mutations-all of which may affect selection on an invading pathogen. Here, we outline the implications that the genetics of sexual dimorphism can have for host-pathogen coevolution and argue that male-female differences influence more than just the environment that a pathogen experiences.
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