Haemoglobin C protects against clinical Plasmodium falciparum malaria

David Modiano (), Gaia Luoni, Bienvenu Sodiomon Sirima, Jacques Simporé, Federica Verra, Amadou Konaté, Elena Rastrelli, Anna Olivieri, Carlo Calissano, Giacomo Maria Paganotti, Leila D'Urbano, Issa Sanou, Alphonse Sawadogo, Guido Modiano and Mario Coluzzi
Additional contact information
David Modiano: Sezione di Parassitologia, WHO Collaborating Centre for Malaria Epidemiology and Control
Gaia Luoni: Sezione di Parassitologia, WHO Collaborating Centre for Malaria Epidemiology and Control
Bienvenu Sodiomon Sirima: Centre National de Recherche et Formation sur le Paludisme, Ministère de la Santé
Jacques Simporé: Centre Medical Saint-Camille
Federica Verra: Istituto Pasteur Fondazione Cenci Bolognetti, University of Rome “La Sapienza”
Amadou Konaté: Centre National de Recherche et Formation sur le Paludisme, Ministère de la Santé
Elena Rastrelli: Sezione di Parassitologia, WHO Collaborating Centre for Malaria Epidemiology and Control
Anna Olivieri: Sezione di Parassitologia, WHO Collaborating Centre for Malaria Epidemiology and Control
Carlo Calissano: Sezione di Parassitologia, WHO Collaborating Centre for Malaria Epidemiology and Control
Giacomo Maria Paganotti: Sezione di Parassitologia, WHO Collaborating Centre for Malaria Epidemiology and Control
Leila D'Urbano: Sezione di Parassitologia, WHO Collaborating Centre for Malaria Epidemiology and Control
Issa Sanou: Service de Pédiatrie, Centre Hospitalier National Yalgado Ouedraogo
Alphonse Sawadogo: Service de Pédiatrie, Centre Hospitalier National Yalgado Ouedraogo
Guido Modiano: Università “Tor Vergata”
Mario Coluzzi: Sezione di Parassitologia, WHO Collaborating Centre for Malaria Epidemiology and Control

Nature, 2001, vol. 414, issue 6861, 305-308

Abstract: Abstract Haemoglobin C (HbC; β6Glu → Lys) is common in malarious areas of West Africa, especially in Burkina Faso1,2. Conclusive evidence exists on the protective role against severe malaria of haemoglobin S (HbS; β6Glu → Val) heterozygosity3, whereas conflicting results for the HbC trait have been reported4,5,6,7,8,9,10 and no epidemiological data exist on the possible role of the HbCC genotype. In vitro studies suggested that HbCC erythrocytes fail to support the growth of P. falciparum11,12 but HbC homozygotes with high P. falciparum parasitaemias have been observed10. Here we show, in a large case–control study performed in Burkina Faso on 4,348 Mossi subjects, that HbC is associated with a 29% reduction in risk of clinical malaria in HbAC heterozygotes (P = 0.0008) and of 93% in HbCC homozygotes (P = 0.0011). These findings, together with the limited pathology of HbAC and HbCC13 compared to the severely disadvantaged HbSS and HbSC genotypes and the low βS gene frequency in the geographic epicentre of βC1,2,14, support the hypothesis that, in the long term and in the absence of malaria control, HbC would replace HbS in central West Africa.

Date: 2001
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DOI: 10.1038/35104556

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