论文部分内容阅读
目的:观察葡萄糖-6-磷酸脱氢酶(G6PD)缺陷症不同表型对恶性疟原虫感染的影响。方法:采用横断面研究的方式,将2012年雨季到马拉博地区医院就诊的2 690名比奥克岛当地居民纳入研究。用显微镜镜检、荧光定量PCR结合熔解曲线法检测疟原虫。用荧光斑点法及PCR-DNA测序鉴定G6PD缺陷症。采用Logistic回归进行关联性分析。结果:该人群的G6PD缺陷症的总发生率为9.22%,基因型均为G6PD*A-(c.202 G>A/c.376 A>G)。G6PD缺陷症体现出强烈的疟疾保护作用(P<0.05);不同性别和表型的G6PD缺陷者中,只有男性半合子对疟疾有保护作用(P<0.05),而女性杂合子组与女性纯合子组均无统计学差异(P>0.05)。结论:G6PD缺陷症的男性半合子表型能够减低恶性疟疾感染的风险,但是其机制尚未明确,有待更深入的研究。
Objective: To observe the effect of different phenotypes of glucose-6-phosphate dehydrogenase (G6PD) on Plasmodium falciparum infection. METHODS: A cross-sectional study was conducted to include 2 690 locals living in Biei Ke, a local hospital visited in the Malabo Regional Hospital during the rainy season of 2012. Plasmodium was detected by microscopic examination, fluorescence quantitative PCR and melting curve method. G6PD deficiency was identified by fluorescent spot assay and PCR-DNA sequencing. Logistic regression was used for correlation analysis. Results: The overall incidence of G6PD deficiency in this population was 9.22% and the genotypes were G6PD * A- (c.202G> A / c.376A> G). G6PD deficiency showed strong protection against malaria (P <0.05). Of the G6PD-deficient individuals of different genders and phenotypes, only male hemizygina had protective effect on malaria (P <0.05), while female heterozygous children and female pure Zizi group had no statistical difference (P> 0.05). Conclusion: The male hemizygous phenotype of G6PD deficiency can reduce the risk of malignant malaria infection. However, its mechanism is not yet clear and remains to be further studied.