Human Molecular Genetics, Vol 6, 1357-1360, Copyright © 1997 by Oxford University Press
D Fernandez-Reyes, AG Craig, SA Kyes, N Peshu, RW Snow, AR Berendt, K Marsh and CI Newbold
The malarial parasite Plasmodium falciparum has acted as a potent selective
force on the human genome. The particular virulence of this organism is
thought to be due to the adherence of parasitised red blood cells to small
vessel endothelium through several receptors, including CD36,
thrombospondin and intercellular adhesion molecule 1 (ICAM-1, CD54), and
parasite isolates differ in their ability to bind to each.
Immunohistochemical studies have implicated ICAM-1 as of potential
importance in the pathogenesis of cerebral malaria, leading us to reason
that if any single receptor were involved in the development of cerebral
malaria, then in view of the high mortality of that complication, natural
selection should have produced variants with reduced binding capacity. We
therefore sequenced the N-terminal domain of ICAM-1 from a number of
Africans and discovered a single mutation present at high frequency.
Genotypes at this locus from samples from a case-control study indicated an
association of the polymorphism with the severity of clinical malaria such
that individuals homozygous for the mutation have increased susceptibility
to cerebral malaria with a relative risk of two. These counterintuitive
results have implications for the mechanism of malaria pathogenesis,
resistance to other infectious agents and transplantation immunology.
ARTICLES
A high frequency African coding polymorphism in the N-terminal domain of ICAM-1 predisposing to cerebral malaria in Kenya
Institute of Molecular Medicine, Nuffield Department of Medicine, John Radcliffe Hospital, Headington, Oxford, UK.
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