Trypanosoma vivax variant antigen diversity is not driven by recombination

What is it about?

African trypanosomes are blood parasites transmitted by tsetse flies that survive in mammals through antigenic variation of their variant antigens (VSG). Recombination is fundamental in other trypanosome species (like Trypanosoma brucei) for both VSG gene switching and for generating antigenic diversity during infections. Trypanosoma vivax is a related, livestock pathogen whose VSG lack the structures that facilitate gene conversion in T. brucei, so the mechanisms underlying its antigenic diversity are poorly understood. Here, we show that species-wide VSG repertoire is limited and broadly conserved across diverse T. vivax clinical strains. We use variant antigen profiling, coalescent approaches and experimental infections to show that recombination plays little role in diversifying T. vivax VSG sequences.

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Photo by Alvaro Reyes on Unsplash

Photo by Alvaro Reyes on Unsplash

Why is it important?

Our 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.