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Protective hemoglobinopathies and Plasmodium falciparum transmission

Nature Genetics volume 42, pages 284–285 (2010)Cite this article

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Human hemoglobin variants are known to protect the host against severe malaria due to P. falciparum. A new study demonstrates that such genetic variation may also be associated with increased transmission of this pathogen from the human host to the Anopheles vector.

Malaria remains a major health burden in endemic countries, with no less than 243 million clinical cases worldwide in 2008 and an estimated 863,000 deaths1. Malaria due to infection with the pathogen P. falciparum has also served as one of the best examples of natural selection in humans, with the association between genetic variation at the beta-globin locus (HBB) and protection from malaria2. On page 328 of this issue, David Modiano and colleagues3 present evidence for an association of particular HBB variants (known to disadvantage the asexual parasite) and enhanced transmission rates of P. falciparum from the human host to the Anopheles vector.

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Figure 1: Genetic variation in the human host may affect transmission as part of the P. falciparum life cycle.

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  1. Geoffrey Pasvol is at Imperial College London, Wellcome Centre for Clinical Tropical Medicine, St Mary's Campus, London, UK.,

    Geoffrey Pasvol

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  1. Geoffrey Pasvol
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Correspondence to Geoffrey Pasvol.

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Pasvol, G. Protective hemoglobinopathies and Plasmodium falciparum transmission. Nat Genet 42, 284–285 (2010). https://doi.org/10.1038/ng0410-284

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