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Studies aimed at studying the biology of protozoan pathogens during mammalian infections have focused on life-cycle stages that can be cultivated in vitro to simulate the bloodstream environment.

However, Trypanosoma brucei, the causative agent of sleeping sickness, not only colonizes the blood, but also interstitial spaces of various organs such as adipose tissue, skin, and brain. In our lab, we study T. brucei - tissue interactions and their implications. We have found that in adipose tissue, parasites alter their gene expression and activate fatty acid β-oxidation.

These results revealed not only an unexpected parasite phenotypic flexibility, but also a globally more heterogenous parasite population. Understanding this flexibility is crucial for improving our knowledge on T. brucei biology, pathogenesis, drug resistance, and disease relapses.

In this seminar, I will discuss the phenotypic adaptation of T. brucei parasites to adipose tissue and our initial progress in understanding tissue-specific invasion mechanisms.

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