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Abstract
BackgroundGlucose‐6‐phosphate dehydrogenase (G6PD) is an essential enzyme that protects red blood cells from oxidative damage. Although G6PD‐deficient alleles appear to confer a protective effect of malaria, the link with clinical protection against Plasmodium infection is conflicting.MethodsA case–control study was conducted on Bioko Island, Equatorial Guinea and further genotyping analysis used to detect natural selection of the G6PD A‐ allele.ResultsOur results showed G6PD A‐ allele could significantly reduce the risk of Plasmodium falciparum infection in male individuals (adjusted odds ratio [AOR], 0.43; 95% confidence interval [CI], 0.20–0.93; p < .05) and homozygous female individuals (AOR, 0.11; 95% CI, 0.01–0.84; p < .05). Additionally, the parasite densities were significantly different in the individuals with different G6PD A‐ alleles and individual levels of G6PD enzyme activity. The pattern of linkage disequilibrium and results of the long‐range haplotype test revealed a strong selective signature in the region encompassing the G6PD A‐ allele over the past 6,250 years. The network of inferred haplotypes suggested a single origin of the G6PD A‐ allele in Africans.ConclusionOur findings demonstrate that glucose‐6‐phosphate dehydrogenase (G6PD) A‐ allele could reduce the risk of P. falciparum infection in the African population and indicate that malaria has a recent positive selection on G6PD A‐ allele.
Highlights
Malaria is a major cause of mortality and morbidity worldwide
Our findings demonstrate that glucose-6-phosphate dehydrogenase (G6PD) A- allele could reduce the risk of P. falciparum infection in the African population and indicate that malaria has a recent positive selection on Glucose-6-phosphate dehydrogenase (G6PD) A- allele
As a major cause of human morbidity, malaria has long been known to be the strongest selective pressure on the human genome over the past 10,000 years. This is the proposition of the “malaria hypothesis”, which posits that certain human genetic polymorphisms, especially those affecting red blood cells (RBCs), have been selected at high frequencies because they provide protection against the effects of malarial infections (Carter & Mendis, 2002)
Summary
Malaria is a major cause of mortality and morbidity worldwide. According to the 2018 World Malaria Report, there were approximately 219 million (95% confidence interval [CI]: 203–262 million) cases of malaria and an estimated 435,000 deaths in 2017, mostly among African children (Tajima, 1989). As a major cause of human morbidity, malaria has long been known to be the strongest selective pressure on the human genome over the past 10,000 years This is the proposition of the “malaria hypothesis”, which posits that certain human genetic polymorphisms, especially those affecting red blood cells (RBCs), have been selected at high frequencies because they provide protection against the effects of malarial infections (Carter & Mendis, 2002). Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway that plays an important role in the body's oxidative defences by governing the formation of nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) from nicotinamide adenine dinucleotide phosphate (Beutler & Duparc, 2007) It could protect RBCs from the harmful effects of reactive oxygen species. We carried out this investigation to search for the evidence of natural selection of the G6PD Aallele by Plasmodium falciparum in the African population on Bioko Island
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