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1 July 2005

Volume 192, Number 1
The Journal of Infectious Diseases 2005;192:178–186
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19201-0025$15.00
DOI: 10.1086/430744
MAJOR ARTICLE

Sickle Cell Trait and the Risk of Plasmodium falciparum Malaria and Other Childhood Diseases

Thomas N. Williams,1,2,3

Tabitha W. Mwangi,1,4

Sammy Wambua,1

Neal D. Alexander,5

Moses Kortok,1

Robert W. Snow,1,2 and

Kevin Marsh1,2

1Kenya Medical Research Institute/Wellcome Trust Programme, Centre for Geographic Medicine Research, Coast, Kilifi District Hospital, Kilifi, Kenya; 2Nuffield Department of Medicine, 3Department of Paediatrics, and 4Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, and 5MRC Tropical Epidemiology Group, London School of Hygiene and Tropical Medicine, London, United Kingdom

Background.The gene for sickle hemoglobin (HbS) is a prime example of natural selection. It is generally believed that its current prevalence in many tropical populations reflects selection for the carrier form (sickle cell trait [HbAS]) through a survival advantage against death from malaria. Nevertheless, >50 years after this hypothesis was first proposed, the epidemiological description of the relationships between HbAS, malaria, and other common causes of child mortality remains incomplete.

Methods.We studied the incidence of falciparum malaria and other childhood diseases in 2 cohorts of children living on the coast of Kenya.

Results.The protective effect of HbAS was remarkably specific for falciparum malaria, having no significant impact on any other disease. HbAS had no effect on the prevalence of symptomless parasitemia but was 50% protective against mild clinical malaria, 75% protective against admission to the hospital for malaria, and almost 90% protective against severe or complicated malaria. The effect of HbAS on episodes of clinical malaria was mirrored in its effect on parasite densities during such episodes.

Conclusions.The present data are useful in that they confirm the mechanisms by which HbAS confers protection against malaria and shed light on the relationships between HbAS, malaria, and other childhood diseases.

Received 20 December 2004; accepted 9 February 2005; electronically published 31 May 2005.

Reprints or correspondence: Dr. T. N. Williams, KEMRI/Wellcome Trust Programme, Centre for Geographic Medicine Research, Coast, PO Box 230, Kilifi District Hospital, Kilifi, Kenya ().

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  • Financial support: Wellcome Trust (grants to T.N.W. and K.M.).

    This article is published with the permission of the director of the Kenya Medical Research Institute.

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