Abstract
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.
Highlights
Human African trypanosomiasis, known as sleeping sickness, is a vector-borne disease caused by two sub-species of protozoan parasites, T. brucei rhodesiense and T. brucei gambiense [1,2]
variable surface glycoproteins (VSGs) molecules are released from the cell surface in two known ways—proteolysis mediated by major surface proteases (MSP) and GPI hydrolysis mediated by phospholipase-C (PLC), both expressed in the bloodstream form of T. brucei
VSG molecules show extraordinary antigenic diversity, comparative analysis of their protein sequences suggests conserved elements that can be a suitable target for the development of drugs against African trypanosomiasis
Summary
Human African trypanosomiasis, known as sleeping sickness, is a vector-borne disease caused by two sub-species of protozoan parasites, T. brucei rhodesiense and T. brucei gambiense [1,2]. In the vector salivary glands, the parasites differentiate into metacyclic trypomastigotes This stage is the infective form for the vertebrate host, characterized by the presence of variable surface glycoprotein (VSG), a dense layer of surface proteins that allows the survival and maintenance of the parasite inside the host by a mechanism of antigenic variation [6]. We discuss the possibility of MSP and PLC proteins being involved in the sophisticated mechanism of antigenic variation, contributing to parasite survival during the maintenance of infection in the mammalian host This intervention model is mainly based on works published by Grandgenett and colleagues [20] and Gruszynski and colleagues [21], where the authors reported that MSP and PLC are involved in the cellular strategy for removing VSG quickly during bloodstream to procyclic T. brucei differentiation.
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