Abstract
Malaria parasites operate antigenicvariation systems to avoid antibody recog-nition, thereby inhibiting their host’scapacity to clear infections [1]. Plasmodi-um falciparum, the most pathogenic of thehuman malaria species, bases immuneevasion on switching expression of ap-proximately 60 var genes. These encodetransmembrane proteins (PfEMP1 anti-gens) on the red blood cell surface, whichallow intraerythrocytic (IE) parasites toadhere to endothelial molecules [2].PfEMP1 proteins are thus not simplyantigenic decoys, but functional vascularadhesion receptors. The disappearance ofolder parasites from the bloodstreamresults from PfEMP1 binding to endothe-lial receptors, a process called sequestra-tion. This enables replicating stages toavoid the dangerous passage through thespleen, the main organ of defence againstblood infection [3]. In this issue, Claessenset al. [4] present new and intriguing dataon how antigenic diversity can be contin-uously generated during persistent malariainfections.
Highlights
Malaria parasites operate antigenic variation systems to avoid antibody recognition, thereby inhibiting their host’s capacity to clear infections [1]
Sequestration affects the course of clinical malaria [5]; and recent studies have linked the binding of specific PfEMP1s to endothelial protein C receptor (EPCR) with severe malaria pathology [6]
The PfEMP1 proteins are encoded by approximately 60 var genes, their extracellular portion encoded by exon 1, a smaller intracellular domain encoded by exon 2
Summary
Malaria parasites operate antigenic variation systems to avoid antibody recognition, thereby inhibiting their host’s capacity to clear infections [1]. Plasmodium falciparum, the most pathogenic of the human malaria species, bases immune evasion on switching expression of approximately 60 var genes These encode transmembrane proteins (PfEMP1 antigens) on the red blood cell surface, which allow intraerythrocytic (IE) parasites to adhere to endothelial molecules [2]. The disappearance of older parasites from the bloodstream results from PfEMP1 binding to endothelial receptors, a process called sequestration This enables replicating stages to avoid the dangerous passage through the spleen, the main organ of defence against blood infection [3]. Sequestration affects the course of clinical malaria [5]; and recent studies have linked the binding of specific PfEMP1s to endothelial protein C receptor (EPCR) with severe malaria pathology [6]. Naıve hosts would be most at risk, and the appearance of novel host receptors, for example the distinctive CSA present on the placental endothelial cells, selects for parasite PfEMP1 variants, which first time mothers would not previously have experienced and to which they had no antibodies [8]
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