The Variant Surface Architecture of African Trypanosomes

African trypanosomes are unicellular, uniflagellated protozoan parasites. They cause African trypanosomiasis or sleeping sickness, a chronic disease in humans as well as in wild and domestic animals. An estimated 50 million people in 36 African countries are at risk of an infection, and a total of about 500,000 newly infected cases per year has been estimated (Smith et al. 1998; Kioy et al. 2004). The disease is caused by two geographically distinct trypanosome subspecies: Trypanosoma bruceirhodesiensein East Africa and T. bruceigambiense in West Africa. Although the two parasites cause different clinical manifestations, both infections are ultimately fatal if untreated (Khaw and Panosian 1995; Kioy et al. 2004).

African trypanosomes are transmitted by tsetse flies and, as extracellular parasites, they multiply within the peripheral blood and the tissue fluids of the infected hosts (Fig. 1). During this bloodstream lifecycle stage, trypanosomes are covered with a layer of approximately 10 million molecules of a glyco-protein species known as variant surface glycoprotein (VSG). VSG molecules have a molecular mass of approximately 60 kDa, they homodimerize and are glycosylphosphatidylinositol (GPI)-anchored within the plasma membrane (Donelson 2003). The VSG surface induces a strong T cell-independent IgM response as well as a T cell-dependent B cell response, which elicits VSG-specific IgG (Sternberg 1998). The parasites, however, evade the host immune system by temporarily expressing different VSG variants (Rudenko et al. 1998). This phenomenon has been termed antigenic variation and has its molecular basis in the surface presentation of structurally polymorphic N-terminal domains of the different VSG variants. The trypanosome genome encodes a repertoire of about 1,000 different vsg genes, but only one VSG is expressed at a given time. Thus, the VSG surface acts as an exclusion barrier for larger molecules, such as antibodies, while its variable characteristics cause the inability of the infected host to clear the infection.

Fig. 1 Cartoon of the main stages of the Trypanosoma brucei lifecycle. The parasites replicate in the blood as slender trypomastigotes and differentiate into so-called stumpy forms at high cell densities. Transmission occurs during the blood meal of a tsetse fly, and the parasite is passaged from the midgut to the salivary glands of the insect vector. The lifecycle is characterized by changes in cell shape, cell cycle, metabolism and surface coat. It is completed after injection of metacyclic-stage parasites into the blood of another host organism

Fig. 1 Cartoon of the main stages of the Trypanosoma brucei lifecycle. The parasites replicate in the blood as slender trypomastigotes and differentiate into so-called stumpy forms at high cell densities. Transmission occurs during the blood meal of a tsetse fly, and the parasite is passaged from the midgut to the salivary glands of the insect vector. The lifecycle is characterized by changes in cell shape, cell cycle, metabolism and surface coat. It is completed after injection of metacyclic-stage parasites into the blood of another host organism

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