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The study of the contribution of human genetics to the risk of severe malaria has a long history, with Haldane in the 1950s reporting a major role of the sickle cell mutation (HbS), in the protection against severe disease (Haldane, 1949). Since then, genetic variants of ┚globin (HbE: Hutagalung et al., 1999; HbC: Agarwal et al., 2000; HbS: Aidoo et al., 2002), ┙-globin (Mockenhaupt et al., 2004), Band 3 protein (Foo et al., 1992), HLA (Hill et al., 1991) and several cytokine loci (Tumor Necrosis Factor-alpha: Knight et al., 1999; Interleukin-12: Morahan et al., 2002a; Interferon-alpha receptor-1: Aucan et al., 2003; Interleukin-4: Gyan et al., 2004) have been demonstrated to confer protection to severe malaria. To date, the majority of studies have been case/control association studies, comparing severe malaria to uncomplicated cases. Due to the fact that Plasmodium falciparum is the etiological agent of severe malaria, all studies have consequently focussed on this parasite. The other congeneric species and notably Plasmodium vivax, can, however, cause severe disease, albeit at a much lower incidence, and warrant an increased research effort (Price et al., 2007).

Human Genetic Contribution to the Outcome of Infection with Malaria Parasites