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Rühli, F.

Publications and source records attributed to Rühli, F..

2 recordsLinked to original sources

Sexually Transmitted Infections Select for Different Levels of Immunocompetence And Reproductive Efforts in The Two Sexes

1.Sex differences in immunity have been described in humans and other mammal species. Females have a lower incidence of infections and non-reproductive malignancies and exhibit higher antibody levels after vaccination. Existing evolutionary explanations are based on differences in reproductive strategies and reaction to extrinsic differences in susceptibility and virulence between the sexes. Here, we test the hypothesis that known differences in the probability of transmission and outcome of sexually transmitted infections contribute to sex differences in immunocompetence. We modelled reproductive and immune investments against a fertility limiting Sexually Transmitted Infection (STI). We show that, in line with previous findings, increased susceptibility selects for tolerance to the parasite while increased virulence selects for resistance against it. Differences in reproductive strategies between the sexes lead to sex differences in immunocompetence, mostly with higher competence in females. Extrinsic differences in susceptibility and virulence between the sexes can augment or alleviate the evolutionary consequences of intrinsic differences depending on their direction and magnitude. This indicates that the selection of sex-specific immune strategies is less predictable than thought before and explains why sex differences in immunity have been found to be not universal and pervasive across animal species.

evolutionary biology

The Evolution of Immune Sensitivity under Immunopathological and Autoimmune Costs

Hosts with high immune sensitivity benefit from rapid recovery but suffer multiple costs thereof. We distinguish between immunopathological costs due to collateral damage and autoimmune costs due to false positives against self. Selection on sensitivity follows different trajectories depending on the cost nature and the overlap degree between host- and parasitic molecular signatures. Increased parasite virulence selects for higher immune sensitivity under immunopathological costs but low sensitivity when the costs are autoimmune, contradicting previous theoretical results. Longer lifespan of the host selects for low sensitivity under immunopathology to avoid accumulated tissue damage. Under autoimmune costs, hosts with a shorter lifespan cannot afford to shorten it further due to autoimmunity and evolve lower immune sensitivity. Longer lifespan selects for high or low sensitivity depending on the presence of immune memory. These results extend our understanding of selection on immune sensitivity and help explain phenomena like the cytokine shock and chronic infections.

evolutionary biology