一個國際科研小組日前發(fā)現(xiàn),，此前一直被人們視為“間日瘧原蟲”免疫人群的非洲人也會感染這種疾病，這一研究結(jié)果顛覆了許多人對此的認識,。
由來自法國,、美國和馬達加斯加的研究人員組成的科研小組在新一期美國《國家科學(xué)院院刊》（PNAS）上發(fā)表報告說，“間日瘧原蟲”是引起瘧疾的“罪魁禍首”——瘧原蟲中的一類,，主要存在于亞洲和南美地區(qū),。此前普遍認為,，紅血球表面缺少名為Duffy蛋白質(zhì)的人群對“間日瘧原蟲”具有天然的免疫力,，因為Duffy是“間日瘧原蟲”的受體，沒有它瘧原蟲就無法進入血液,。大多數(shù)非洲人的血液都呈Dffy陰性,，即不具備此類蛋白質(zhì)，這也在一定程度上解釋了非洲很少有“間日瘧原蟲”感染病例的原因,。
然而,，研究人員日前對馬達加斯加部分居民進行觀察后發(fā)現(xiàn)，一些呈Duffy陰性的居民也感染了“間日瘧原蟲”,，這說明后者已成功繞過Duffy蛋白質(zhì),，通過另一條“道路”進入了紅血球，Duffy已不再是“間日瘧原蟲”傳播的必要條件,，但研究人員目前還不清楚其中的具體機制,。
研究人員說，全球平均每年都會發(fā)現(xiàn)7000萬到8000萬例“間日瘧原蟲”感染病例,，新的發(fā)現(xiàn)改變了人們此前對“間日瘧原蟲”免疫人群的看法,。(生物谷Bioon.com)
JEM：可抑制瘧原蟲和弓形蟲的分子
Nature Genetics：瘧原蟲遺傳的基因圖譜被繪制
瘧原蟲形態(tài) Morphology
生物谷推薦原文出處：
PNAS doi:10.1073/pnas.0912496107
Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people
Didier Ménarda,b,1,2, Céline Barnadasa,c,1, Christiane Bouchierd, Cara Henry-Halldinc, Laurie R. Grayc, Arsène Ratsimbasoae, Vincent Thoniera, Jean-Fran?ois Carodf, Olivier Domarlea, Yves Coling, Olivier Bertrandg, Julien Picotg, Christopher L. Kingc,h, Brian T. Grimbergc, Odile Mercereau-Puijalonb,2, and Peter A. Zimmermanc,2
Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*BESBES) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption–elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffy-independent P. vivax invasion of human erythrocytes.
