Abstract
African trypanosomosis is a debilitating disease of great medical and socioeconomical importance. It is caused by strictly extracellular protozoan parasites capable of infecting all vertebrate classes including human, livestock, and game animals. To survive within their mammalian host, trypanosomes have evolved efficient immune escape mechanisms and manipulate the entire host immune response, including the humoral response. This report provides an overview of how trypanosomes initially trigger and subsequently undermine the development of an effective host antibody response. Indeed, results available to date obtained in both natural and experimental infection models show that trypanosomes impair homeostatic B-cell lymphopoiesis, B-cell maturation and survival and B-cell memory development. Data on B-cell dysfunctioning in correlation with parasite virulence and trypanosome-mediated inflammation will be discussed, as well as the impact of trypanosomosis on heterologous vaccine efficacy and diagnosis. Therefore, new strategies aiming at enhancing vaccination efficacy could benefit from a combination of (i) early parasite diagnosis, (ii) anti-trypanosome (drugs) treatment, and (iii) anti-inflammatory treatment that collectively might allow B-cell recovery and improve vaccination.
Highlights
African trypanosomes are strictly extracellular single-celled protozoan parasites belonging to the genus Trypanosoma, which cause debilitating diseases in humans and livestock and significantly affect the socioeconomic development of sub-Saharan Africa [1]
To design and maintain future control strategies, it is important to indicate that T. b. gambiense is an anthroponotic disease with a minor role for animal reservoirs that accounts for 98% of the reported Human African trypanosomosis (HAT) cases and causes a chronic, gradually progressing disease, whereby the late meningoencephalitic stage is not reached before months or even years of infection [10, 15]
Within the tsetse fly, the parasites are covered by a procyclin coat, and only when they differentiate into the metacyclic forms (MCFs), they express a metacyclic variant surface glycoprotein (VSG) coat [70]
Summary
African trypanosomes are strictly extracellular single-celled protozoan parasites belonging to the genus Trypanosoma, which cause debilitating diseases in humans and livestock and significantly affect the socioeconomic development of sub-Saharan Africa [1]. About 70 million people distributed over a surface of one and a half million square kilometers are estimated to be at risk for contracting sleeping sickness in Africa [2]. The distribution of African trypanosomes coincides mostly with the distribution of the habitat of the hematophagic insect vector, i.e., the tsetse “fly” (Glossina sp.), with tsetse meaning “fly” in the Tswana language of Southern Africa [3]. Human African trypanosomosis (HAT) or sleeping sickness is caused by Trypanosoma brucei gambiense (west and central Africa) and Trypanosoma brucei rhodesiense (eastern and southern Africa) [4, 5]
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