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variant surface glycoprotein.
Trypanosoma brucei evades the immune system by switching between Variant Surface Glycoprotein (VSG) genes.
Variant surface antigen (VSA) transcripts were detected by optimized probes representing the VSA genes of three geographically distinct strains.
The data has been analyzed with reference to variant surface antigens, encoded by the var, rifin and stevor gene families.
Acquisition of antibodies against these variant surface antigens may protect women and their offspring.
The enzyme is not important for release of GPI-anchored variant surface glycoprotein (VSG) from the plasma membrane [8], [9].
This susceptibility is associated with placental sequestration of parasitised red blood cells expressing pregnancy-specific variant surface antigens.
For example, telomeric repression in trypanosomes has been demonstrated for genes encoding variant surface molecules (VSG) in T. brucei [27].
In the mammalian host, bloodstream forms of the parasite are covered by a coat consisting of variant surface glycoprotein (VSG).
Plasmodium falciparum infected red blood cells (iRBC) express variant surface antigens (VSA) of which VAR2CSA is involved in placental sequestration and causes pregnancy-associated malaria (PAM).
Of critical importance for the bloodstream form trypanosome is a dense protective layer of Variant Surface Glycoprotein (VSG), which shields invariant surface receptors from recognition [1].
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