Human genetic polymorphisms and asymptomatic Plasmodium falciparum malaria in Gabonese schoolchildren

Human genetic polymorphisms and asymptomatic Plasmodium falciparum malaria in Gabonese schoolchildren
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DOI:
10.4269/ajtmh.2003.68.186
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发表时间:
2003-02-01
影响因子:
3.3
通讯作者:
Krishnamoorthy, R
Krishnamoorthy, R
中科院分区:
医学4区
文献类型:
--
作者:
Mombo, LE;Ntoumi, F;Krishnamoorthy, R

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一些研究将注意力集中在宿主遗传因素与严重疟疾易感性/抗性之间的关系上。然而,关于宿主遗传因素在无症状疟疾(一种无临床症状的低级别恶性疟原虫感染)中的作用的信息缺乏。在这项研究中,我们调查了宿主(人类)遗传多态性(葡萄糖-6-磷酸脱氢酶[G6PD]、甘露糖结合凝集素[MBL]、肿瘤坏死因子α [TNFalpha](-308)和(-238)一氧化氮合酶2 [NOS2](-954))与158名加蓬学童无症状恶性疟原虫感染的患病率和特征之间的潜在关系。我们发现G6PD A(-)杂合雌性(74例中有18例)无症状疟疾患病率较低(38.9%对67.3%,经卡方检验P = 0.03)。TNFalpha杂合的儿童(-238)(156例中的25例)携带大量不同的感染寄生虫基因型(2.5对1.99;方差F = 3.05)。MBL、TNFalpha(-308)或NOS2多态性与无症状疟疾之间无统计学意义的相关性。将无症状型的数据与其他形式的文献数据相结合,我们得出结论,G6PD A(-)杂合雌性对所有形式的恶性疟原虫疟疾都有保护作用,而TNFalpha(- 238a)等位基因对临床疟疾具有保护作用。
Several studies have focused their attention on the relationship between host genetic factors and susceptibility/resistance to severe malaria. However, there is a paucity of information concerning the role of host genetic factors in asymptomatic malaria, a form of low-grade Plasmodium falciparum infection without clinical symptoms. We investigated in this study the potential relationship between the host (human) genetic polymorphisms (glucose-6-phosphate dehydrogenase [G6PD], mannose binding lectin [MBL], tumor necrosis factor alpha [TNFalpha](-308) and (-238) nitric oxide synthase 2 [NOS2](-954)) and the prevalence and profile of asymptornatic P. falciparum infection in 158 Gabonese schoolchildren. We found that G6PD A(-) heterozygous females (18 of 74) have a low prevalence of asymptornatic malaria (38.9% versus 67.3%; P = 0.03, by chi-square test). Children heterozygous for TNFalpha(-238) (25 of 156) carry high number of diverse infecting parasite genotypes (2.5 versus 1.99; variance F = 3.05). No statistically significant association was found between MBL, TNFalpha(-308) or NOS2 polymorphisms and asymptomatic malaria. Upon combining our data on asymptornatic forms with those from the literature for others forms, we conclude that G6PD A(-) heterozygous females are protected against all forms of P. falciparum malaria, and that the TNFalpha(-238A) allele confers protection against clinical malaria.