The two mechanisms for antigenic variation in Trypanosoma brucei are independent processes

Abstract

Antigenic switching in Trypanosoma brucei can occur either by the production of a telomeric copy of a variant surface glycoprotein (VSG) gene through a gene conversion mechanism or by the nonduplicative activation of a telomeric VSG gene. The 5 VSG gene telomeric copy that is expressed in IsTaR 1 variant antigenic type (VAT) 5 is retained in an inactive state following an antigenic switch to VAT A5. This inactive telomeric 5 VSG gene copy is absent following independent single antigenic switches to VATs 1A5 and 11A5. The inactive 5 VSG gene does not appear to have been replaced with the newly expressed VSG gene. Thus, inactive telomeric VSG genes that are capable of being expressed can be lost, presumably through gene conversion to new VSG genes. These results suggest that gene conversion of an inactive VSG gene does not obligately activate the new VSG gene. We conclude that the gene conversion and telomeric activation mechanisms for antigenic switching are separate and independent processes.