Oxidation in Red Cell Disorders Research Unit, Department of Clinical Microscopy, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand.
Department of Molecular Tropical Medicine and Genetics, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.
J Infect Dis. 2022 Apr 1;225(7):1238-1247. doi: 10.1093/infdis/jiab484.
Protection against Plasmodium falciparum is observed in a population deficient in glucose-6-phosphate dehydrogenase (G6PD), particularly in African and Mediterranean regions. However, such protection remains unknown among G6PD-deficient individuals in Southeast Asia.
In this study, we assessed the invasion and maturation of P falciparum K1 in a culture of erythrocytes isolated from Thai subjects carrying Viangchan (871G > A) and Mahidol (487G > A).
We found that the parasites lost their ability to invade hemizygous and homozygous G6PD-deficient erythrocytes of Viangchan and Mahidol variants in the second and third cycles of intraerythrocytic development. It is interesting to note that P falciparum parasites selectively grew in erythrocytes from hemi- and homozygous genotypes with normal G6PD activity. Moreover, externalization of phosphatidylserine upon P falciparum infection was significantly increased only in Viangchan hemizygous variant cells.
This study is the first to show that blockage of invasion in long-term culture and potentially enhanced removal of parasitized erythrocytes were observed for the first time in erythrocytes from Viangchan and Mahidol G6PD-deficient individuals.
在葡萄糖-6-磷酸脱氢酶（G6PD）缺乏的人群中观察到对恶性疟原虫（Plasmodium falciparum）的保护作用，特别是在非洲和地中海地区。然而，在东南亚 G6PD 缺乏的个体中，这种保护作用尚不清楚。
在这项研究中，我们评估了携带 Viangchan（871G＞A）和 Mahidol（487G＞A）突变的泰国个体分离的红细胞培养物中恶性疟原虫 K1 的入侵和成熟情况。
我们发现，寄生虫在第二和第三轮红细胞内发育周期中丧失了入侵 Viangchan 和 Mahidol 变体杂合子和纯合子 G6PD 缺乏红细胞的能力。有趣的是，恶性疟原虫寄生虫选择性地在具有正常 G6PD 活性的半合子和纯合子基因型的红细胞中生长。此外，只有在 Viangchan 杂合变体细胞中，恶性疟原虫感染时磷脂酰丝氨酸的外化显著增加。
这项研究首次表明，在 Viangchan 和 Mahidol G6PD 缺乏个体的红细胞中，长期培养中观察到入侵阻断和潜在增强的寄生虫清除。
