Although extracellular throughout their lifecycle, trypanosomes are able to persist despite strong host immune responses through a process known as antigenic variation involving a large, highly diverse family of surface glycopro- tein (VSG) genes, only one of which is expressed at a time. Previous studies have used mathematical models to investigate the relationship between VSG switching and the dynamics of trypanosome infections, but none have explored the role of multiple VSG expression sites or the contribution of mosaic gene conversion events involving VSG pseudogenes.