Associations between α+‐Thalassemia and Plasmodium falciparum Malarial Infection in Northeastern Tanzania
1Centre for Medical Parasitology, Institute for International Health, Immunology, and Microbiology, and 2Department of Forensic Genetics, Institute of Forensic Medicine, University of Copenhagen, Copenhagen, Denmark; 3Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom; 4National Institute for Medical Research, Tanga Medical Research Centre, Tanga, and 5Joint Malaria Programme, Moshi, Tanzania
Background.
The 2 most common hemoglobinopathies, sickle cell trait and α+‐thalassemia, confer partial resistance to fatal forms of malaria, but the molecular basis for this protection is still not understood. Examination of the relationship between these traits and malaria transmission intensity may provide insights into the protection afforded.
Methods.The distribution of the 2 traits was assessed among children resident in 13 villages in the Eastern Arc Mountains in Tanzania, where Plasmodium falciparum transmission intensity is closely correlated with altitude. Associations between the prevalence of the 2 traits and malariometric indices were investigated by logistic regression. Short tandem repeat (STR) microsatellite allele frequencies were used to assess population substructuring.
Results.The frequency of α+‐thalassemia ranged from 10%–25% in high‐altitude villages (>1200 m) to 45%–55% in low‐altitude villages (<600 m). The carriage rate of α+‐thalassemia decreased by 
12% per 100‐m increase in altitude (
) and was 50% lower among those with patent parasitemia than among uninfected individuals (
). The prevalence of the sickle cell trait was lower than that of α+‐thalassemia (range, 0%–14%) and was significantly associated with village altitude only (
). STR allele frequencies were similar in all villages.
Conclusions.In this malaria‐endemic region of Tanzania, α+‐thalassemia is common and clearly associated with P. falciparum transmission intensity. There was no evidence of population substructuring, and the results are suggestive of selection of the α3.7 allele by malaria.
Received 22 December 2006; accepted 9 March 2007; electronically published 20 June 2007.
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Online publication date: 1-Oct-2008.
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Potential conflicts of interest: none reported.
Presented in part: 4th MIM Pan‐African Malaria Conference, Yaoundé, Cameroon, 13–18 November 2005 (poster 590B).
Financial support: UK Medical Research Council (grant G9901439 to the study); Danish International Development Agency, Danish Ministry of Foreign Affairs (grant 91203 to A.E.); Wellcome Trust Research Training Fellowship (grant 063516 to C.J.D.).