Trypanosomosis is a very important and complicated haemo-protozoan infection caused by a eukaryotic unicellular parasite trypanosomes. The parasite mainly found in the blood and other tissues of vertebrates. African trypanosomes established adaptive strategies to avoid the host immune system primarily via antigenic variation where the parasite changes its variant surface glycoprotein (VSG) coat to evade the host immune responses. Metacyclic form and bloodstream trypanosomes’ total cell surface including the flagellum covered with a coat to render overall protection against non-specific host resistance mechanisms. There are two mechanisms where variant-types could develop; the first one is through either there could exist in all trypanosomes a series of genetic loci or the second one is a single antigen-determining locus could mutate in one or more individual parasites to generate VSG. In addition to VSG expression, switching is another mechanism in trypanosomes for escaping host immune response. One of the distinguishing features of the trypanosome infections is a remarkable suppression of the immune responses that lead to high susceptibility to opportunistic infections. There are numerous functions of the VSG coat, such as, it helps to escape specific immune response, causes the parasite to resist complement lysis, host tissues synthesis of auto-antibody by molecular mimicry and mediate persistent cytokine production. On account of the factors that regulate antigenic variations are difficult to totally comprehend and the variation mechanism itself, vaccine development against this disease become virtually impossible. In addition, a safe and effective vaccine production would be next to impossible due to presence of extremely complex host immune evasion mechanisms.
Keywords: Antigenic variation; Immunosuppression; Trypanosome;Vaccine; Variant surface glycoprotein