Developed a within-host infection model integrating theory and experiments to distinguish between tolerance and resistance mechanisms. Provided a practical experimental framework for explaining individual differences in susceptibility to infection, a methodological foundation applied in subsequent work.

We studied the phenotypic plasticity of Drosophila gut in response to glucose level in diet.

We tested the effects of circadian temperature fluctuations on a series of thermal plasticity traits in a model of adaptive seasonal plasticity, the Bicyclus anynana butterfly.

A central problem with biomedicine is to understand why two individuals exposed to seemingly identical infections may have radically different clinical outcomes. Using the Drosophila melanogaster model, we analyse in depth, both through functional genetics and mathematical modelling, the main determinants that underlie the stochastic outcome of infection.

In this “essay” we propose for the first time the idea that the sexual dimorphism of diseases may be the result of the specific adaptation of parasites to the sex of their host. Similarly, as organisms adapt to the environment to which they are most frequently exposed, parasites can adapt to the sex they encounter most frequently (e.g., either because males and females are exposed differently, or because one sex is more easily infected than another due to immune differences). As a result, parasites behave differently depending on the sex they infect.