Inward route for malaria

can invade erythrocytes via a glycophorin C-mediated pathway.

Tudor Toma
Dec 8, 2002

A deletion in the glycophorin C gene (GYPC ∆ex3) results in a negative Gerbich (Ge) blood group common in Papua New Guinea where malaria is hyperendemic. Ge negativity is correlated to reduced susceptibility to malaria infection, but how this protection arises has been unclear. In December 9 Nature Medicine, Alexander G. Maier and colleagues at The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia, show that GYPC mediates a principal Plasmodium falciparum invasion pathway into human erythrocytes (Nature Medicine doi:10.1038/nm807, December 9, 2002).

Maier et al. examined the interaction between erythrocytes and parasites in which the gene for erythrocyte-binding antigen 140 (EBA140) had been disrupted. They observed that the erythrocyte receptor for EBA140 is glycophorin C (GYPC) and that EBA140–GYPC interaction mediates a P. falciparum invasion pathway into human erythrocytes. In addition, they show that EBA140 does not bind to GYPC in Ge-negative erythrocytes, nor...

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