For many years, the Molecular Parasitology Laboratory has been mainly devoted to the study of the mechanisms of adaptation of African trypanosomes, parasites that cause sleeping sickness in man and the nagana disease in cattle. Previous lab studies have shown that the lipoprotein APOL1, found in human serum, can defeat trypanosomes. However, the subspecies T. b. rhodesiense can neutralize the effects of APOL1 thanks to a protein, termed SRA.

David Pérez-Morga, Etienne Pays and collaborators want to decipher the relationship between APOLs and SRA. They have also found that the APOL1 structure is very similar to that of some members of the apoptotic BCL2 protein family. The researchers’ hypothesis is that APOLs are responsible for controlling programmed cell death of certain human cells under inflammatory conditions, e.g. when encountering a pathogen. New lab results seem to confirm this theory.

Other results suggest that APOL1 variant forms, allowing some West African populations to resist T. b. rhodesiense infection, progressively trigger necrosis of podocytes. This can cause chronic kidney disease, frequently observed in those populations.

Spokesperson

David-Pérez-Morga
Molecular Parasitology Cell
Faculty of Sciences

Dates
Created on August 31, 2018