CD36 c.1264 T>G Null Mutation Impairs Acquisition of IgG Antibodies to Plasmodium falciparum MSP1-19 Antigen and is Associated with Higher Malaria Incidences in Tanzanian Children

D. Kajeguka, C. Mwanziva, M. Daou, A. Ndaro, S. Matondo, E. Mbugi, W. Dolmans, J. Chilongola
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Polymorphisms in genes that encode crucial signalling molecules have been proposed as factors that influence susceptibility to, and outcome of malaria. We studied the role of a mutation, c.1264 T>G, that causes CD36 deficiency on IgG responses to MSP-119 antigen and malaria incidence. Children were genotyped for the c.1264 T>G mutation at the beginning of the study using PCR-RFLP. IgG levels [optical density (OD) readings] and per cent seropositivity to MSP-119 were determined at baseline by ELISA. Children were followed for 12 months for acquisition of anti-MSP-119 IgG antibody and malaria incidence. We observed a significant increase in the production of anti-MSP-119 IgG antibody in normal and heterozygous children during the 12 months of follow-up, but not in homozygous mutants. Normal children had a significantly lower malaria incidence rate compared to other genotypes (χ2 = 115.59; P < 0.01). We conclude that the presence of the c.1264 T>G mutation that leads to CD36 deficiency is closely associated with reduced IgG production and higher malaria incidence. It is most likely that deficiency of CD36 which is known to modulate dendritic cell function suppresses the production of protective IgG antibodies directed to Plasmodium falciparum MSP-119 antigen, which predisposes to the acquisition of clinical malaria in children.