title: Human red blood cell polymorphisms and malaria.
abstract: Genetic factors are a major determinant of child survival in malaria endemic countries. Identifying which genes are involved and how they affect the malaria disease risk potentially offers a powerful mechanism through which to learn more about the host-parasite relationship. The past few years have seen significant progress towards achieving this goal for some of the best-known malaria resistance genes that determine the structure or function of red blood cells: Gerbich blood group antigen negativity; polymorphisms of the complement receptor genes (most notably CR1); Southeast Asian ovalocytosis; pyruvate kinase deficiency; haemoglobin E; the sickle cell trait; and alpha-thalassaemia are all examples. The challenge for the future must be to translate such advances into fresh approaches to the prevention and treatment of malaria.
authors.affiliation: KEMRI/Wellcome Trust Collaborative Programme, Kilifi, Kenya. twilliams@kilifi.mimcom.net
authors.forename: Thomas N
authors.initials: TN
authors.lastname: Williams
mesh_terms: D001457:Anion Exchange Protein 1, Erythrocyte / Q000235:genetics; D004912:Erythrocytes / Q000378:metabolism / Q000469:parasitology*; D006446:Hemoglobin E / Q000502:physiology; D006451:Hemoglobin, Sickle / Q000502:physiology; D006453:Hemoglobinopathies / Q000235:genetics; D006801:Humans; D008288:Malaria / Q000235:genetics* / Q000517:prevention & control*; D011110:Polymorphism, Genetic; D017463:Receptors, Complement 3b / Q000235:genetics; D013789:Thalassemia / Q000235:genetics; D014759:Viral Envelope Proteins / Q000235:genetics
chemical_list: D001457:Anion Exchange Protein 1, Erythrocyte; D006451:Hemoglobin, Sickle; D017463:Receptors, Complement 3b; D014759:Viral Envelope Proteins; C038535:glycoprotein gC, herpes simplex virus type 1; D006446:Hemoglobin E