Erythrocyte polymorphisms and malaria parasite invasion in Papua New Guinea.
Plasmodium falciparum merozoites engage the erythrocyte surface through several receptor (host)-ligand (parasite) interactions during a brief exchange that results in parasite invasion of the red blood cell. Tens of thousands of these events occur during the initial cycle of blood-stage infections but advance towards billions as the parasite becomes visible to microscopists attempting to diagnose the underlying cause of illness in febrile patients. Advancing blood-stage infection leads to massive proportions of erythrocytes that rupture during repetitive cycles of asexual reproduction. As the infection leads to illness, non-immune or semi-immune individuals can suffer from life-threatening consequences of severe malarial anemia that play a leading role in pathogenesis. Through natural selection, some erythrocyte membrane polymorphisms are likely to have reduced the invasion success of the P. falciparum merozoite and increased the fitness of the human host population.
Zimmerman
Peter A
PA
Center for Global Health and Diseases, School of Medicine, Case Western Reserve University, W147D 2109 Adelbert Road, Cleveland, OH 44106-4983, USA. paz@po.cwru.edu
Patel
Sheral S
SS
Maier
Alexander G
AG
Bockarie
Moses J
MJ
Kazura
James W
JW
D000818:Animals; D001789:Blood Group Antigens / Q000235:genetics; D004910:Erythrocyte Membrane / Q000469:parasitology; D004912:Erythrocytes / Q000469:parasitology*; D005838:Genotype; D006021:Glycophorins / Q000235:genetics; D006801:Humans; D008024:Ligands; D008288:Malaria / Q000097:blood* / Q000235:genetics / Q000469:parasitology; D008565:Membrane Proteins / Q000235:genetics; D010219:Papua New Guinea; D010961:Plasmodium / Q000502:physiology; D011110:Polymorphism, Genetic
D001789:Blood Group Antigens; D006021:Glycophorins; D008024:Ligands; D008565:Membrane Proteins