Abstract
Erythrocytes infected with the mature forms of the malarial parasite Plasmodium falciparum do not circulate in the peripheral blood but instead adhere to postcapillary venular endothelium (1). The phenomenon is analogous in many ways to lymphocyte adhesion to endothelium in that it is mediated by specific receptor-ligand interactions and must take place under shear flow conditions. Unlike lymphocytes, however, the infected erythrocytes do not transmigrate, but remain adherent for a period of approximately 24 h, during which time parasite development continues, until rupture of the erythrocyte and the release of the next generation of blood-stage parasites. Cytoadherence is thought to be an important contributor to the pathogenesis of severe malaria, since high local concentrations of parasitized cells may significantly affect flow, deplete the blood of metabolites, and release toxic products. Several complications of severe disease, such as cerebral malaria, are characterized by dense packing of infected erythrocytes in the vascular beds of affected organs (2), implying that the ability of the infected cells to localize in deep-tissue vasculature has an important bearing on the clinical outcome.
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