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Background  Innate immunity plays a crucial role in the host defense against malaria including  Plasmodium falciparum  malaria in pregnancy, but the roles of the various underlying genes and mechanisms predisposing to the disease are poorly understood.    Methods  98 single-nucletoide polymorphisms were genotyped in a set of 17 functionally related genes of the complement system in 145 primiparous Ghanaian women with placental malaria, defined by placental parasitaemia or malaria pigment, and as a control, in 124 non-affected primiparae.    Results  Placental malaria was significantly associated with SNPs in the lectin pathway genes  MBL2, MASP2, FCN2  and in  properdin . In particular, the main African mannose-binding lectin deficiency variant ( MBL2* G57E, rs1800451) increased the odds of placental malaria (OR 1.6; permuted p-value 0.014). In contrast, a common  MASP2  mutation (R439H, rs12085877), which reduces the activity of MBL-MASP2 complexes occurred in 33% of non-affected women and in 22% primiparae with placental malaria (OR 0.55, permuted  p -value 0.020).    Conclusions  Excessive complement activation is of importance in the pathogenesis of placental malaria by mediating inflammation, coagulation, and endothelial dysfunction. Mutated MBL and MASP2 proteins could have direct intrinsic effects on the susceptibility to placental malaria, in addition to their roles in regulation of downstream complement activation.

Mutations of complement lectin pathway genes MBL2 and MASP2 associated with placental malaria