My Research area is infection biology, with a particular focus on the host-parasite interactions that determine whether or not an infection leads to severe disease. The model organisms that I use to study this problem are trypanosomes, which are single-celled parasites that infect humans and animals in sub-Saharan Africa, and mice, which during trypanosome infections mimic many of the clinical signs observed in humans and cattle. Both of these organisms have inherent features, encoded by genes, which make this an ideal system for studying host-parasite interactions. Different strains of mouse reproducibly vary in the severity of disease when infected with trypanosomes, suggesting that there is an inherited genetic basis to susceptibility. Indeed, work has identified regions of the mouse genome that contain a gene determining mouse susceptibility. My work exploits the fact that some trypanosome strains cause more severe disease than others; similar to mice this suggests a trypanosome genetic basis influencing disease severity. I previously identified a region in the trypanosome genome that contains a gene that determines whether a parasite causes more severe clinical signs. The first aim of my work is to identify this gene and characterise how its protein product exerts the effect on the host. The second aim is to use infections with hosts that differ in susceptibility and parasites that vary in pathogenesis to ask: what is the more important influence on disease outcome, host susceptibility or parasite virulence? Thirdly, do the same host-parasite interactions play similar roles in the different trypanosomes that cause human and animal disease? The ultimate aim is to understand how an infection progresses from the initial inoculation of the parasite to the host displaying symptoms of disease. If we understand how disease develops, we can hope to design intelligent interventions that will prevent serious clinical signs, and reduce the disease burden of this parasite.