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Host genetic factors probably determine both susceptibility to infection and severity of damage by pathogens. A large number of polymorphisms have now been implicated in the onset, progression, and outcome of malaria infection, seeming to influence the ability of the host immune response to control the infection. These include:
those associated with haemoglobinopathies1
those within the major histocompatibility complex (HMC), including HLA class I and class II and the tumour necrosis factor promoter
those within genes not associated with HMC, such as ICAM-1, CD36, and possibly the gene for nitric oxide synthase2
probably the gene for apolipoprotein E (APOE), as our recent data suggest, and upon which we comment below.3
APOE has three main alleles, types 2, 3, and 4, resulting in six possible genotypes; it codes for the protein apoE, which is involved in transport of lipids in the blood and the central nervous system.
Finding that APOE-ε2 homozygous Ghanaian infants were more likely to be infected with the malaria protozoon at a very young …
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