Abstract
Background The deep vascular sequestration of parasitized erythrocytes is a central pathological event in falciparum malaria. Variant surface antigens are encoded mainly by three multi-copy gene families, namely, var, stevor ,a ndrifin. Var is one of the most important families that plays a crucial role in antigenic variation and immune evasion. Clinical and epidemiological studies have shown that severe or complicated malaria is manifested in a limited number of patients. This indicates that a subset of these multigene families could be determinants in the manifestation of different malaria phenotypes. Recent studies have indicated the possible role of stevor (sub-telomeric variable open read), a multi-gene family, in erythrocyte invasion, antigenic variation and host cell modification, of infected erythrocytes. In this study, we describe the repertoire and diversity of members of the stevor multigene family in patients with complicated and uncomplicated malaria in India.
Highlights
The deep vascular sequestration of parasitized erythrocytes is a central pathological event in falciparum malaria
A maximum likelihood phylogeny was constructed in order to understand the genetic repertoire of members of the stevor multigene family in severe and
The repertoire and diversity of the stevor multigene family varied between all four geographical regions of the Indian subcontinent
Summary
The deep vascular sequestration of parasitized erythrocytes is a central pathological event in falciparum malaria. Variant surface antigens are encoded mainly by three multi-copy gene families, namely, var, stevor, and rifín. Clinical and epidemiological studies have shown that severe or complicated malaria is manifested in a limited number of patients. This indicates that a subset of these multigene families could be determinants in the manifestation of different malaria phenotypes. Recent studies have indicated the possible role of stevor (sub-telomeric variable open read), a multi-gene family, in erythrocyte invasion, antigenic variation and host cell modification, of infected erythrocytes.
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