Parasitism relies on the ability of an organism to exploit its host. Trypanosoma brucei is a unicellular parasite responsible for a fatal disease in humans (sleeping sickness), and for a chronic disease in cattle (nagana) in Sub-Saharan Africa. Our group is interested in understanding the cellular and molecular mechanisms employed by T. brucei to be an effective parasite. Our current projects focus on two main interests:

1. TISSUE TROPISM– Our lab recently demonstrated that the adipose tissue is a major parasite reservoir during a mouse infection and that parasites functionally adapt to the tissue. These unexpected observations raised many questions: how do parasites move between tissues? What is the selective advantage to accumulate in this tissue? Are parasites equally susceptible to drug treatment? How do parasites enter/exit the tissues? What is the extravascular contribution to the dynamics of parasite transmission?

2. ANTIGENIC VARIATION– A long-standing interest of our group is to understand the mechanisms that govern antigenic variation, a process that allows trypanosomes to escape the host immune response. We are currently studying the importance of non-coding RNAs and epigenetic modifications on the regulation of genes underlying antigenic variation.

Host-parasite interaction, extravascular parasites, adipose tissue, antigenic variation

Trypanosoma brucei