Shimizu Hana, Tamam Moedrik, Soemantri Augustinus, Ishida Takafumi
Department of Human Ecology, School of International Health, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Department of Child Health, Faculty of Medicine, Diponegoro University, Semarang, Indonesia.
J Hum Genet. 2005;50(8):420-424. doi: 10.1007/s10038-005-0271-7. Epub 2005 Jul 30.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency and Southeast Asian ovalocytosis (SAO) caused by a 27-bp deletion in the band 3 gene (Band3Delta 27) are well-documented genetic traits resistant to malarial diseases; however, relationships between these traits and asymptomatic malaria infection hitherto had not been investigated. Filter-blotted blood samples were collected from a total of 210 healthy individuals, 100 males and 110 females, aged 6-17 years, in Sumba island, Indonesia, to survey for the presence of Plasmodium parasites, G6PD activity and the Band3Delta 27 mutation. Presence of P. falciparum and/or P. vivax was identified in 25 subjects (11.9%). In all, 24 subjects (11.4%) showed Band3Delta 27 heterozygously. In males and females, eight and nine subjects, respectively, showed G6PD deficiency. There was no significant difference in the prevalence of asymptomatic malaria infection between individuals with or without these traits (P>0.05). No alterations in the prevalence of asymptomatic malaria infection suggest that parasite invasion into erythrocytes is unlikely to be a target phase in which the two polymorphisms demonstrate possible protective effects against malaria.
葡萄糖-6-磷酸脱氢酶（G6PD）缺乏症以及由3号带基因27碱基对缺失（Band3Delta 27）引起的东南亚卵形红细胞增多症（SAO）是有充分文献记载的抗疟疾遗传性状；然而，这些性状与无症状疟疾感染之间的关系此前尚未得到研究。从印度尼西亚松巴岛210名6至17岁的健康个体（100名男性和110名女性）中采集滤膜印迹血样，以检测疟原虫的存在、G6PD活性以及Band3Delta 27突变。在25名受试者（11.9%）中检测到恶性疟原虫和/或间日疟原虫。总共有24名受试者（11.4%）表现为Band3Delta 27杂合子。男性和女性中分别有8名和9名受试者表现出G6PD缺乏症。具有或不具有这些性状的个体之间无症状疟疾感染的患病率没有显著差异（P>0.05）。无症状疟疾感染患病率没有变化表明，寄生虫侵入红细胞不太可能是这两种多态性发挥抗疟疾保护作用的目标阶段。
