Data analysis
malaria, placental infection
MALARIA, REGRESSION, PLACENTAL INFECTION
One hundred and eighty-nine SNPs of interest from the maternal data (95 SNPs) and the children data (94 SNPs) were selected for analysis. Genes previously published from this study in relation with malaria [The freeware programmes PSPP (A Poisson model was used to correlate the number of primary cases (defined as above) with genotypes of SNPs of interest, while using the factors and covariates of: (1) maternal age; (2) parity; (3) child’s sex; (4) use of insecticide-treated nets (ITNs); (5) use of indoor residual spraying (IRS); (6) in utero placental infection (defined by examining histological samples of the placenta); and (7) intervention group. This model treats each genotype category independently (additive model) and was applied to the cumulative data available at the fourth year after birth, which constitutes three time-points corresponding to the children’s ages of 2, 3, and 4 years (the first-year data was omitted due to the influence of maternal immunological protection and administering of interventions during that period). For each SNP, the major allele homozygotes present in this study was defined as the reference genotype. To account for child genotypes confounding effects in maternal genotype results, all significant maternal SNPs were subjected to the Poisson analysis once more, this time including the corresponding child SNP as a co-factor. All results were corrected for multiple testing using a false discovery rate (FDR) adjustment.All SNPs identified via the Poisson regression as being associated with primary clinical malaria cases were analysed together with other SNPs in the same gene as part of a gene-centric haplotype. Haplotypes most likely associated with malaria were identified using the haplotype trend regression (HTR) model available in R [