Membrane modifications in erythrocytes parasitized by Plasmodium falciparum.
Plasmodium falciparum malaria parasites invade human red blood cells and immediately begin making significant alterations to the structure of the erythrocyte. These alterations facilitate the movement of nutrients into, and waste products and parasite-derived proteins out of the cell to meet the needs of the growing parasite. A tubovesicular membrane network extending from the parasite vacuole membrane probably has a central role in the transport processes. The parasite also modifies the erythrocyte membrane itself in a way that not only changes its permeability but also places parasite-derived proteins in knob-like protrusions at the cell surface. These proteins enable the parasite to adhere to endothelial cells and thereby avoid clearance from the blood stream by the spleen. Antigenic variation of these proteins allows parasitized erythrocytes to vary their phenotype and produce a sustained and chronic malaria infection. Study of the molecular processes that underlie these parasite-induced modifications of the host red blood cell will lead to improved understanding of malaria pathogenesis and, perhaps, suggest new approaches against the disease.
Deitsch
K W
KW
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-0425, USA.
Wellems
T E
TE
D000818:Animals; D000953:Antigens, Protozoan / Q000235:genetics / Q000378:metabolism; D001692:Biological Transport; D002448:Cell Adhesion; D004910:Erythrocyte Membrane / Q000235:genetics / Q000378:metabolism / Q000469:parasitology* / Q000502:physiology; D006790:Host-Parasite Interactions; D016778:Malaria, Falciparum / Q000378:metabolism / Q000473:pathology; D008565:Membrane Proteins / Q000235:genetics / Q000276:immunology / Q000502:physiology; D008954:Models, Biological; D010963:Plasmodium falciparum / Q000472:pathogenicity*
D000953:Antigens, Protozoan; D008565:Membrane Proteins