Malaria susceptibility and CD36 mutation

Timothy J. Aitman (), Lisa D. Cooper, Penny J. Norsworthy, Faisal N. Wahid, Jennefer K. Gray, Brian R. Curtis, Paul M McKeigue, Dominic Kwiatkowski, Brian M. Greenwood, Robert W. Snow, Adrian V Hill and James Scott
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Timothy J. Aitman: Molecular Medicine Group, MRC Clinical Sciences Centre, and Imperial College Genetics and Genomics Research Institute, Hammersmith Hospital
Lisa D. Cooper: Molecular Medicine Group, MRC Clinical Sciences Centre, and Imperial College Genetics and Genomics Research Institute, Hammersmith Hospital
Penny J. Norsworthy: Molecular Medicine Group, MRC Clinical Sciences Centre, and Imperial College Genetics and Genomics Research Institute, Hammersmith Hospital
Faisal N. Wahid: Molecular Medicine Group, MRC Clinical Sciences Centre, and Imperial College Genetics and Genomics Research Institute, Hammersmith Hospital
Jennefer K. Gray: Molecular Medicine Group, MRC Clinical Sciences Centre, and Imperial College Genetics and Genomics Research Institute, Hammersmith Hospital
Brian R. Curtis: Blood Center of Southeastern Wisconsin, Medical College of Wisconsin
Paul M McKeigue: London School of Hygiene and Tropical Medicine
Dominic Kwiatkowski: MRC Laboratories
Brian M. Greenwood: MRC Laboratories
Robert W. Snow: KEMRI Coastal Research Unit
Adrian V Hill: Wellcome Trust Centre for Human Genetics, University of Oxford
James Scott: Molecular Medicine Group, MRC Clinical Sciences Centre, and Imperial College Genetics and Genomics Research Institute, Hammersmith Hospital

Nature, 2000, vol. 405, issue 6790, 1015-1016

Abstract: Abstract A critical step in infection by Plasmodium falciparum, the microorganism that causes the most severe form of malaria, is the adhesion of parasitized red blood cells to capillary endothelium. The human protein CD36 is a major receptor for P. falciparum-infected red blood cells1,2 and may contribute to the disease by sequestering infected red blood cells1,2 and inhibiting the immune response to the parasite3. We have found that African populations contain an exceptionally high frequency of mutations in CD36. Unexpectedly, these mutations that cause CD36 deficiency are associated with susceptibility to severe malaria, suggesting that the presence of distinct CD36 mutations in Africans and Asians4,5,6 is due to some selection pressure other than malaria.

Date: 2000
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DOI: 10.1038/35016636

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