Fowkes Freya J I, Michon Pascal, Pilling Lynn, Ripley Ruth M, Tavul Livingstone, Imrie Heather J, Woods Caira M, Mgone Charles S, Luty Adrian J F, Day Karen P
The Peter Medawar Building for Pathogen Research, Department of Zoology, University of Oxford, UK.
Malar J. 2008 Jan 3;7:1. doi: 10.1186/1475-2875-7-1.
The protection afforded by human erythrocyte polymorphisms against the malaria parasite, Plasmodium falciparum, has been proposed to be due to reduced ability of the parasite to invade or develop in erythrocytes. If this were the case, variable levels of parasitaemia and rates of seroconversion to infected-erythrocyte variant surface antigens (VSA) should be seen in different host genotypes.
To test this hypothesis, P. falciparum parasitaemia and anti-VSA antibody levels were measured in a cohort of 555 asymptomatic children from an area of intense malaria transmission in Papua New Guinea. Linear mixed models were used to investigate the effect of alpha+-thalassaemia, complement receptor-1 and south-east Asian ovalocytosis, as well as glucose-6-phosphate dehydrogenase deficiency and ABO blood group on parasitaemia and age-specific seroconversion to VSA.
No host polymorphism showed a significant association with both parasite prevalence/density and age-specific seroconversion to VSA.
Host erythrocyte polymorphisms commonly found in Papua New Guinea do not effect exposure to blood stage P. falciparum infection. This contrasts with data for sickle cell trait and highlights that the above-mentioned polymorphisms may confer protection against malaria via distinct mechanisms.
人类红细胞多态性对恶性疟原虫的保护作用被认为是由于该寄生虫在红细胞内入侵或发育的能力降低。如果是这样的话，在不同宿主基因型中应该会观察到不同水平的寄生虫血症以及针对感染红细胞变异表面抗原（VSA）的血清转化速率。
为了验证这一假设，对来自巴布亚新几内亚疟疾传播密集地区的555名无症状儿童进行了队列研究，测量了他们的恶性疟原虫血症水平和抗VSA抗体水平。使用线性混合模型研究α+地中海贫血、补体受体1、东南亚椭圆形红细胞增多症，以及葡萄糖-6-磷酸脱氢酶缺乏症和ABO血型对寄生虫血症和针对VSA的年龄特异性血清转化的影响。
没有一种宿主多态性与寄生虫感染率/密度以及针对VSA的年龄特异性血清转化存在显著关联。
在巴布亚新几内亚常见的宿主红细胞多态性不会影响恶性疟原虫血液阶段感染的暴露情况。这与镰状细胞性状的数据形成对比，并突出表明上述多态性可能通过不同机制赋予对疟疾的保护作用。
