Abstract
African trypanosomes (Trypanosoma) are vector-borne haemoparasites that survive in the vertebrate bloodstream through antigenic variation of their Variant Surface Glycoprotein (VSG). Recombination, or rather segmented gene conversion, is fundamental in Trypanosoma brucei for both VSG gene switching and for generating antigenic diversity during infections. Trypanosoma vivax is a related, livestock pathogen whose VSG lack structures that facilitate gene conversion in T. brucei and mechanisms underlying its antigenic diversity are poorly understood. Here we show that species-wide VSG repertoire is broadly conserved across diverse T. vivax clinical strains and has limited antigenic repertoire. We use variant antigen profiling, coalescent approaches and experimental infections to show that recombination plays little role in diversifying T. vivax VSG sequences. These results have immediate consequences for both the current mechanistic model of antigenic variation in African trypanosomes and species differences in virulence and transmission, requiring reconsideration of the wider epidemiology of animal African trypanosomiasis.
Highlights
African trypanosomes (Trypanosoma) are vector-borne haemoparasites that survive in the vertebrate bloodstream through antigenic variation of their Variant Surface Glycoprotein (VSG)
Superficially like the more familiar Trypanosoma brucei and Trypanosoma congolense, T. vivax is distinct in morphology and motility[6], cellular ultrastructure[7,8] and genetic repertoire, with regard to cell surface-expressed genes[9,10]
Sequence repeats known to facilitate gene conversion in T. brucei were absent from the T. vivax reference genome, suggesting that the T. brucei-based paradigm of antigenic variation might not apply to other species[10]
Summary
African trypanosomes (Trypanosoma) are vector-borne haemoparasites that survive in the vertebrate bloodstream through antigenic variation of their Variant Surface Glycoprotein (VSG). Superficially like the more familiar Trypanosoma brucei (the species responsible for Human African trypanosomiasis) and Trypanosoma congolense (another livestock parasite), T. vivax is distinct in morphology and motility[6], cellular ultrastructure[7,8] and genetic repertoire, with regard to cell surface-expressed genes[9,10]. Most conspicuously, it has a simpler life cycle in tsetse flies, lacking a procyclic stage in the insect midgut, and can be transmitted noncyclically by other genera of haematophagous flies[6]. Sequence repeats known to facilitate gene conversion in T. brucei were absent from the T. vivax reference genome, suggesting that the T. brucei-based paradigm of antigenic variation might not apply to other species[10]
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