Adherence of Plasmodium falciparum-infected erythrocytes (PRBCs) to the mic
rovascular endothelium of specific organs and consequent sequestration is b
elieved to be responsible for the development of malaria pathology. A numbe
r of studies have shown that cell adhesion molecules expressed on the surfa
ce of endothelial cells mediate the adherence. Recent studies indicate that
a subpopulation of PRBCs adhere to chondroitin 4-sulfate (C4S). This adhes
ion can be effectively inhibited by C4S oligosaccharides. In pregnant women
, the placenta specifically selects C4S-adherent PRBCs, and thus these phen
otypes multiply and sequester in the intervillous spaces. Over successive p
regnancies, women develop a protective humoral response to the C4S-adhesion
phenotype. Disruption of C4S-mediated PRBCs adhesion using either a C4S ol
igosaccharide mimetic or an antiC4S-adhesion Vaccine can be an efficient st
rategy for the treatment of malaria caused by C4S-adherent P. falciparum.