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Aim: The present study aimed to evaluate the Plasmodium falciparum genetic diversity according to the host hemoglobin and G6PD genetic variants during the course of malaria in infected children aged from 2 to 10 years and living in endemic area in Burkina Faso. Study Design: The study was designed as a longitudinal follow up conducted between May 2015 and February 2016 in Banfora health district, Burkina Faso. Methodology: We included 136 subjects (73 males and 63 females; age range from 2-10 years). Blood thick and thin film was done by capillary blood. Venous blood was collected for DNA extraction. Malaria diagnosis was done by microscopy. Human and parasite DNA were extracted based on Qiagen kit procedure. Then, hemoglobin and G6PD were genotyped by RLFP-PCR while the msp1, msp2 and eba175 genes were typed by a nested PCR. All PCR products were analyzed by electrophoresis on a 1.5-2% agarose gel and alleles categorized according to the molecular weight. Results: The prevalence of hemoglobin type was 19.11% for abnormal hemoglobin and 80.9% for normal hemoglobin carriage. The prevalence of G6PD type was 91.18% for normal and 8.82% for G6PD deficiency carriage, respectively. The prevalence of msp1 allelic families was 81.60%, 80.80% and 67.20% for k1, ro33 and mad20 respectively while for msp2 gene, fc27 and 3D7 allelic family the prevalence was 70.53% and 69.64% respectively. The eba175 allelic families’ distribution showed 77.31% and 40.21% for fcr3 and Camp respectively. There was no difference in multiplicity of infection (MOI) according to hemoglobin genotypes and G6PD types. We found that k1 was the predominant allelic family of msp1 in normal hemoglobin genotype (AA) and normal G6PD type. The mixed infection of eba175 was statistically higher in abnormal hemoglobin (p=0.04). There was no statistical difference between fcr3 and camp prevalence excepted in G6PD deficient type. The polymorphism results showed that the prevalence of 450 bp in fc27 was statistically significantly higher in normal hemoglobin variant carriers (AA) than abnormal hemoglobin carriers (p=2.10 -4)). However, the prevalence of 350 bp in fc27 was statistically higher in normal G6PD than deficient G6PD carriers (p=0.034). Conclusion: Our result showed that the distribution of msp1 and eba75 polymorphism could be influenced by hemoglobin and G6PD variants. These results suggest that hemoglobin and G6PD could influence P. falciparum genetic diversity.

Aims: The aim of this study was to assess the impact of hemoglobin polymorphisms and G6PD deficiency on the course of uncomplicated malaria infection in children aged from 2 to 10 years in Burkina Faso. Study Design: The study was conducted as a longitudinal study in Banfora health district. A total of 150 children aged from 2 to 10 years was enrolled and followed up between May 2015 and February 2016. Blood samples were collected at four different time points: before infection (Visit 1), during asymptomatic parasitemia (Visit 2), during symptomatic parasitemia (Visit 3) and three weeks after treatment (Visit 4). Clinical examination, hematology parameters and malaria diagnosis using microscopy were performed. Hemoglobin and G6PD typing were done using PCR-RFLP. Hemoglobin AA genotypes were defined as normal hemoglobin while Hemoglobin AC, AS and SS were defined as abnormal hemoglobin (hb non-AA). Results: The prevalence of hemoglobin (hb) genotypes was 81.21% for AA while hb non-AA genotypes were estimated at 18.79% (12.08% for hbAC, 6.04% for hbAS and 0.67% for HbSC). The prevalence of G6PD genotypes was 89.26% and 10.74% for normal G6PDn and G6PD deficiency respectively. The prevalence of asymptomatic carriers of P. falciparum was not affected neither by the genotypes of Hemoglobin, nor by the G6PD deficiency. Conversely, the risks of developing uncomplicated malaria in G6PD deficiency (G202A) group, was significantly lower (p = 0.04). The results showed a significant difference (p˂0.0001) in the means of P. falciparum parasite densities between asymptomatic and symptomatic phase in Hemoglobin AA genotypes carriers while the means of parasite density was comparable in non-Hemoglobin AA carriers. Conclusion: Our study showed that G6PD deficiency protects against clinical malaria while P. falciparum parasite density increasing was correlated with carrying hemoglobin genotypes AA.