Abstract

Plasmodium falciparum malaria remains a major cause of mortality and severe morbidity in large parts of the world. Most of those who die or become seriously ill from the disease are young children or pregnant women. The adhesion of infected erythrocytes (IEs) in various tissues—a process called sequestration—is thought to be key to the pathogenesis of P. falciparum malaria and is therefore a topic of high research priority. Sequestration is thought to be the result of interaction between parasite-encoded variant surface antigens (VSA) on the outer membrane of IEs and a range of host receptors. In this issue of The American Journal of Pathology, Muthusamy et al1 demonstrate that IEs that can accumulate in the placenta and thereby cause a severe form of malaria known as placental or pregnancy-associated malaria (PAM) bind to chondroitin sulfate proteoglycans (CSPG) but not to another host receptor, hyaluronic acid (HA), which has also been implicated in the pathogenesis of PAM.

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