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Human African trypanosomes: challenges posed to the human immune system.
Abstract
Human infection by either Trypanosoma brucei gambiense (Tbg) or Trypanosoma brucei rhodesiense (Tbr) and the establishment of disease is made possible by the intermittent switching of their variant surface
glycoprotein (VSG) and expression of serum resistance associated (SRA) protein (by Tbr) which nullifies the lytic action of the normal human serum. The ability to switch expression from one VSG to the other is recognized to be the major mechanism that permits the parasite to evade the otherwise efficient host antibody, hence preventing parasite elimination and allowing the establishment of a chronic infection. These changes were reported to: disable the host’s capacity to mount a protective anti-parasite antibody response and prevent the development of effective B-cell memory against encountered variant antigenic parasite types (VATs). Both B cell-mediated antibody response and the Th1 cell responses leading to the production of interferon-gamma (IFN-ϒ) are required for maximum host resistance to trypanosomes, with IFN-ϒ acting to induce macrophage trypanolytic and trypanostatic activities. High levels of both tumor necrosis factor alpha (TNFα) and interleukin 10 (IL-10) have been associated with trypanosomal infection. Trypanosomal genetics (including the parasite’s intrinsic characteristics), human immune response polymorphisms and geographical locations are important elements that describe the severity or mildness of HAT. As the parasite devices ways to evade the
human immune system, and in the absence of a suitable vaccine, surveillance, prompt diagnosis and treatment with available drugs and vector control efforts will go along way in reducing the incidence of HAT.
Keywords: African trypanosomes, Variant surface glycoprotein, Serum resistance associated (SRA) protein, Trypanosomal genetic polymorphisms, Immune response polymorphisms
glycoprotein (VSG) and expression of serum resistance associated (SRA) protein (by Tbr) which nullifies the lytic action of the normal human serum. The ability to switch expression from one VSG to the other is recognized to be the major mechanism that permits the parasite to evade the otherwise efficient host antibody, hence preventing parasite elimination and allowing the establishment of a chronic infection. These changes were reported to: disable the host’s capacity to mount a protective anti-parasite antibody response and prevent the development of effective B-cell memory against encountered variant antigenic parasite types (VATs). Both B cell-mediated antibody response and the Th1 cell responses leading to the production of interferon-gamma (IFN-ϒ) are required for maximum host resistance to trypanosomes, with IFN-ϒ acting to induce macrophage trypanolytic and trypanostatic activities. High levels of both tumor necrosis factor alpha (TNFα) and interleukin 10 (IL-10) have been associated with trypanosomal infection. Trypanosomal genetics (including the parasite’s intrinsic characteristics), human immune response polymorphisms and geographical locations are important elements that describe the severity or mildness of HAT. As the parasite devices ways to evade the
human immune system, and in the absence of a suitable vaccine, surveillance, prompt diagnosis and treatment with available drugs and vector control efforts will go along way in reducing the incidence of HAT.
Keywords: African trypanosomes, Variant surface glycoprotein, Serum resistance associated (SRA) protein, Trypanosomal genetic polymorphisms, Immune response polymorphisms
