title: Innate resistance to malaria: the intraerythrocytic cycle.
abstract: The human innate resistance to P. falciparum malaria is based on genetic features that affect several stages of the intraerythrocytic cycle of the plasmodia. HbS, HbE and alpha and beta thalassemia (in addition to G-6PD deficiency) are protective to the carriers, because they inhibit the intraerythrocytic growth period, and in the case of AS red cells, in addition, parasitosis make them detectable expeditiously by the spleen. Blood group polymorphisms can interfere with red cell invasion by plasmodia. HbC belongs to a special category, since it apparently interferes with the cycle at the moment of cell lysis and release of merozoites. Finally, ovalocytosis observed in South East Asia, which most likely corresponds to a cytoskeleton or membrane protein defect, protects from malaria by inhibiting invasion. It should be kept in mind that many of these red cell defects might protect individuals in the critical first 5 years of life by retarding the switch of HbF to adult hemoglobin, since the HbF containing red cells are less than hospitable to the parasite.
authors: Division of Hematology, Albert Einstein College of Medicine, Bronx, NY 10461.
authors: R L
authors: RL
authors: Nagel
mesh_terms: D000818:Animals; D004912:Erythrocytes / Q000469:parasitology / Q000502:physiology*; D006446:Hemoglobin E / Q000502:physiology; D006451:Hemoglobin, Sickle / Q000502:physiology; D006453:Hemoglobinopathies / Q000097:blood*; D006801:Humans; D007113:Immunity, Innate; D008288:Malaria / Q000097:blood* / Q000276:immunology; D009154:Mutation; D010963:Plasmodium falciparum / Q000472:pathogenicity*; D013789:Thalassemia / Q000097:blood*
chemical_list: D006451:Hemoglobin, Sickle; D006446:Hemoglobin E