Variant antigen diversity in Trypanosoma vivax is not driven by recombination

摘要: African trypanosomes are vector-borne haemoparasites that cause trypanosomiasis in humans and animals. Parasite survival the bloodstream depends on immune evasion, achieved by antigenic variation of Variant Surface Glycoprotein (VSG) coating trypanosome cell surface. Recombination, or rather directed gene conversion, is fundamental Trypanosoma brucei, as both a mechanism VSG switching generating diversity during infections. vivax related, livestock pathogen also displaying variation, but whose lack key structures necessary for conversion T. brucei. Thus, this study tests long-standing prediction has more restricted repertoire. Here we show global repertoire broadly conserved across diverse clinical strains. We use sequence mapping, coalescent approaches experimental infections to recombination plays little, if any, role diversifying sequences. These results explain interspecific differences disease, such propensity self-cure, indicate either an alternate evasion else distinct transmission strategy reduces its reliance long-term persistence. The driving immediate consequences current mechanistic model species virulence strategy, requiring us reconsider wider epidemiology animal trypanosomiasis.