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VSG stands for variant surface glycoprotein, the major surface component of the protozoan parasite Trypanosoma brucei while it exists in the blood and tissues of its mammalian host. Transmitted by the bite of the tsetse (Glossina spp.), T. brucei infects mammals in sub-Saharan Africa. Two subspecies, T. brucei gambiense and T. b. rhodesiense, infect humans, causing human African trypanosomiasis, a fatal disease when left untreated. Another subspecies, T. b. brucei, infects animals, causing animal African trypanosomiasis, a disease whose effect on domestic livestock poses a huge economic burden to sub-Saharan Africa. The parasite lives extracellularly in the blood and tissues of its mammalian hosts, and VSG is key to long-term infection in this harsh environment. This glycophosphatidylinositol (GPI)-anchored glycoprotein is extremely abundant on the parasite surface, with an estimated 10 copies covering the plasma membrane (Fig 1). VSG gets the “V” in its name from T. brucei's large genomic repertoire of VSG-encoding genes. During an infection, the parasite undergoes antigenic variation in which it “switches” expression of the VSG, drawing from a genomic repertoire of>1,000 VSG-encoding genes (the precise size of this repertoire probably varies between subspecies). In T. b. brucei, about 80% of this repertoire consists of incomplete genes or pseudogenes [1,2]. A VSG mRNA is transcribed from one of ~15 telomeric bloodstream expression sites (BESs), while all other BESs remain transcriptionally silent [3]. Thus, only one VSG covers the parasite surface at any time, except when the parasite is in the process of VSG switching. To change the expressed VSG, transcription can be turned off at one BES and turned on at another (in situ switching), or new VSG genes can be moved into a BES by gene conversion [4]. VSG switching can also occur by telomere exchange, in which VSGs are swapped through recombination between two BESs [4].

Masters of Disguise: Antigenic Variation and the VSG Coat in Trypanosoma brucei