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Background: Glucose‐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. Methods: A case–control study was conducted on Bioko Island, Equatorial Guinea and further genotyping analysis used to detect natural selection of the G6PD A‐ allele. Results: Our 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. Conclusion: 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 G6PD A‐ allele. [ABSTRACT FROM AUTHOR]

Objective: Drug resistance against Plasmodium falciparum has been recognized as the crucial obstacle to curbing mortality and morbidity from malaria. To investigate the distribution and pattern of multidrug resistance 1 (pfmdr1) gene polymorphisms in P. falciparum, isolates collected from the malaria high-endemic Bioko Island, Equatorial Guinea., Methods: Blood samples were collected from 217 patients with P. falciparum malaria during rainy season in 2012 on Bioko Island. These samples were extracted using Chelex to obtain parasite DNA. Nest-polymerase chain reaction (PCR) and sequencing were employed to detect mutations (N86Y, E130K, Y184F, S1034C, N1042D, V1109I, and D1246Y) and haplotypes in pfmdr1 gene., Results: A total of 151 samples were successfully detected for pfmdr1 mutations from the 217 patients. Pfmdr1 mutations were found in 91·39% (138/151) P. falciparum isolates. However, no mutation at 130 and 1109 was identified from these samples. Four haplotypes coding 86, 184, 1034, 1,042, and 1,246 were found including NYSND, YYSND, NFSND, and YFSND, which accounted for 8·61% (13/151), 2·65% (4/151), 29·80% (45/151), and 58·94% (89/151), respectively., Conclusions: Our results exhibited hypersensitivity to lumefantrine (LU) and mefloquine (MQ) and resistance to chloroquine (CQ) and amodiaquine (AQ) in P. falciparum isolates from Bioko Island. This information will be useful for anti-malarial drug policy in Equatorial Guinea.