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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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.

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This page is a summary of: Variant antigen diversity in Trypanosoma vivax is not driven by recombination, Nature Communications, February 2020, Springer Science + Business Media, DOI: 10.1038/s41467-020-14575-8.
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