THE 2 MECHANISMS FOR ANTIGENIC VARIATION IN TRYPANOSOMA-BRUCEI ARE INDEPENDENT PROCESSES

Antigenic switching in T. 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 VATA5. 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. Apparently, gene conversion of an inactive VSG gene does not obligately activate the new VSG gene. The gene conversion and telomeric activation mechanisms for antigenic switching may be separate and independent processes.