Getting down to malarial nuts and bolts: the interaction between Plasmodium vivax merozoites and their host erythrocytes.
Of the four Plasmodium species that routinely cause malaria in humans, Plasmodium falciparum is responsible for the majority of malaria mortality and consequently gets most of the headlines. Outside Africa, however, more malaria cases are caused by its distant cousin Plasmodium vivax, resulting in a daunting morbidity and economic burden for countries across Asia and the Americas. Plasmodium life cycles are complex, but the symptoms and pathology of malaria occur during the blood phase, when merozoites recognize and invade erythrocytes, initiating a developmental programme that culminates in lysis of the erythrocyte and release of multiple daughter merozoites. P. vivax merozoites are dependent on a single host cell receptor for erythrocyte invasion, the Duffy antigen receptor for chemokines, and humans that do not express this receptor on the surface of their erythrocytes are immune to P. vivax infection. This essential receptor-ligand interaction is addressed from both the host and parasite side in two papers in this issue of Molecular Microbiology, with important implications for plans to develop a P. vivax vaccine.
Rayner
Julian
J
Division of Geographic Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA. jrayner@uab.edu
D000818:Animals; D004912:Erythrocytes / Q000378:metabolism / Q000469:parasitology*; D006790:Host-Parasite Interactions; D006801:Humans; D008288:Malaria / Q000235:genetics / Q000378:metabolism / Q000469:parasitology*; D010966:Plasmodium vivax / Q000276:immunology / Q000378:metabolism / Q000502:physiology*