Trypanosome Antigenic Variation—A Heavy Investment in the Evasion of Immunity

Publisher Summary A range of relapsing diseases of humans and other animals are caused by Trypanosoma brucei (T. brucei), including human sleeping sickness of chronic and acute forms. Similar diseases are caused in livestock by Trypanosoma congolense and Trypanosoma vivax. All these species are transmitted by tsetse, although some have spread outside the tsetse belt through through simpler transmission modes. The relapsing nature and the chronicity of the trypanosomiases are a direct consequence of antigenic variations. T. brucei establishes infection in each host type (or anatomical niche) through multiplicative stages that include the long slender form in the mammalian host and the procyclic and epimastigote forms in the tsetse. This chapter describes the antigenic variations of trypanosome. Antigenic variations in trypanosome probably begins with the reassignment of a surface receptor to a more passive coating role. As the coat comes in direct conflict with the immune system, antigenic switching at a high rate becomes necessary, and this is most readily achieved by the opportune use of an unstable DNA sequence that allows the gene-duplication system to operate. The initial few variant genes expand into an enormous repertoire, and the trypanosome subsequently evolves some more elaborate structures and systems.