Pattern of Variant Surface Glycoprotein Coating in Nascent Metacyclic Trypanosoma Brucei in the Salivary Glands of Glossina Morsitans

Abstract

The African trypanosomes are protected against their mammalian hosts’ non-specific and specific defence mechanisms by a glycoprotein coat. The antigenic nature of the glycoprotein can be changed by a gene-switching mechanism enabling the parasite population to avoid destruction by host antibodies, and a succession of variable antigen types (VATs) appears in the blood of an infected animal as the parasitaemia fluctuates. New VATs arise regardless of the host mounting an immune response. These can be detected by immunofluorescence or immune lysis reactions as “heterotypes” (minority populations) in a “homotype” population (i.e. one composed predominantly of trypanosomes belonging to the same VAT). In infections of Trypanosoma brucei, homotype VATs appear in a semi-predictable sequence, but what selects out a particular heterotype to become the next homotype is not clear, and whether the genes coding for the various variant-surface glycoproteins (VSGs) are activated in a particular sequence is not known (reviewed Boothroyd 1985, Barry 1986).