Data from: Mosaic VSGs and the scale of Trypanosoma brucei antigenic variation

A main determinant of prolonged Trypanosoma brucei infection, and hence
transmission and success of the parasite, is the interplay between host
acquired immunity and antigenic variation of the parasite variant surface
glycoprotein (VSG) coat. About 0.1% of trypanosome divisions produce a
switch to a different VSG through differential expression of an archive of
hundreds of silent VSG genes and pseudogenes, but the patterns and extent
of the trypanosome diversity phenotype, particularly in chronic infection,
are unclear. We applied longitudinal VSG cDNA sequencing to estimate
variant richness and test whether pseudogenes contribute to antigenic
variation. We show that individual growth peaks can contain at least 15
distinct variants, are estimated computationally to comprise many more,
and that antigenically distinct ‘mosaic’ VSGs arise from segmental gene
conversion between donor VSG genes or pseudogenes. The potential for
trypanosome antigenic variation is probably much greater than VSG archive
size; mosaic VSGs are core to antigenic variation and chronic infection.