Moreno, Cláudia Jassica GonçalvesTemporão, AdrianaTorres, TaffarelSilva, Marcelo Sousa2021-05-022021-05-022019-03-021661-6596PURE: 18015645PURE UUID: 20711509-107f-4019-8b90-358ba9ee7f1cScopus: 85064208217PubMed: 30934540PubMedCentral: PMC6471236WOS: 000464325300003http://hdl.handle.net/10362/116745This research was funded by GHTM-UID/multi/04413/2013 (FCT-Portugal) and Grant number 019/2013 (Capes-Brazil).The protozoan Trypanosoma brucei, responsible for animal and human trypanosomiasis, has a family of major surface proteases (MSPs) and phospholipase-C (PLC), both involved in some mechanisms of virulence during mammalian infections. During parasitism in the mammalian host, this protozoan is exclusively extracellular and presents a robust mechanism of antigenic variation that allows the persistence of infection. There has been incredible progress in our understanding of how variable surface glycoproteins (VSGs) are organised and expressed, and how expression is switched, particularly through recombination. The objective of this manuscript is to create a reflection about the mechanisms of antigenic variation in T. brucei, more specifically, in the process of variable surface glycoprotein (VSG) release. We firstly explore the mechanism of VSG release as a potential pathway and target for the development of anti-T. brucei drugs.733812engAntigenic variationMajor surface proteasePhospholipase-CTrypanosoma bruceiVariable surface glycoproteinCatalysisMolecular BiologySpectroscopyComputer Science ApplicationsPhysical and Theoretical ChemistryOrganic ChemistryInorganic Chemistryreview10.3390/ijms20061484https://www.scopus.com/pages/publications/85064208217