Trypanosoma and Plasmodium have members that can evade the human immune system by frequently changing their surface proteins
Antigenic variation in P. falciparum is driven by PfEMP1/var. The other gene families' members, rif, stevor, and surfin, which encode the proteins RIFINS, STEVOR, and SURFIN, respectively, go through clonal variation, which makes them useful in evading the host immune response.
By frequently changing the thick layer of variable surface glycoprotein (VSG) on the cell surface, Trypanosoma brucei parasites successfully escape the host immune system. The monoallelic expression of VSGs is strictly regulated in each parasite. On the trypomastigotes, the VSG proteins (60 kDa) produce a surface coating that is 12–15 nm thick. Through significant antigenic diversity, the VSGs allow the trypomastigotes to sidestep the immune system of the mammalian host.
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