Most infectious diseases have a sexually dimorphic outcome. We investigate the reasons for this not only with a host-centered view but also by considering that pathogens adapt to the most commonly encountered sex.
Infection outcome depends on the success of the parasite within its host. With theoretical and empirical approaches, we study what influences pathogen dynamics and its implication on symptoms.
In the interest of better understanding the differences between sexes, we have studied sexual selection and conflict. We did so in two ways:
I- Parthenogenetic species produce mainly daughters without males. We study selection during the rare events of sexual reproduction in Daphnia.
II- Seminal fluid proteins are generally considered male tools to manipulate females. We investigated the growing hypothesis that seminal fluid proteins are important signals for females to adjust their egg-laying and mating decisions, and thus help reduce sexual conflict.
Genetic variation is the raw material for evolution. We pertain to study how phenotypic plasticity generates phenotypic heterogeneity, its genetic basis, and how it can explain variation in host-parasite interactions.