電影中的詹姆斯·邦德曾使用了一系列窮兇極惡的小暗器,，從有毒的飛鏢鋼筆到能夠發(fā)射激光的手表,。然而最近發(fā)現(xiàn)的一個屬于類鼻疽桿菌——導致東南亞人和澳大利亞北部居民罹患類鼻疽的罪魁禍首——的蛋白質卻比所有這一切更加致命。這項研究表明,，這種名為BPSL1549的蛋白質可以使細菌的毒性提高100倍,。
類鼻疽又被稱為“越南定時炸彈”,，這種疾病在越南戰(zhàn)爭后引起了人們的極大關注,。隨著美軍直升機在這個亞熱帶國家頻繁起降,，螺旋槳激起的塵埃將士兵和飛行員暴露在曾隱藏在土壤中的病原體面前。
類鼻疽的癥狀與許多疾病很類似,，包括皮膚感染和肺部化膿,。但有一些患者卻會演變出嚴重的敗血癥，在一些地區(qū),，這種疾病的死亡率甚至高達40%,。
為了找到其中的原因，英國謝菲爾德大學的分子生物學家Stuart Wilson和同事對類鼻疽桿菌的一種蛋白質BPSL1549進行了研究,，后者與在大腸桿菌中常見的一種酶很類似,。這種大腸桿菌蛋白質是一種細胞毒素。
為了搞清這種酶的作用,，研究人員分別向兩組小鼠體內注射了攜帶BPSL1549及沒有攜帶這種蛋白質的類鼻疽桿菌,。結果顯示，前者殺死的嚙齒動物數(shù)量是后者的100倍,。Wilson說,，可見，雖然這種微生物也會產生其他一些毒素,，但BPSL1549無疑是其中最毒的。
研究人員在最新出版的美國《科學》雜志上報告了這一研究成果。
類鼻疽是由類鼻疽桿菌所致的地方性傳染病,，流行于東南亞和澳大利亞北部等熱帶地區(qū),。人主要是通過接觸含有致病菌的水和土壤，經破損的皮膚而受感染 ,。該病潛伏期一般為3～5天,，但也有感染后數(shù)月、數(shù)年,，甚至20年發(fā)病的情況,。此類病例常因外傷或其他疾病而誘發(fā)。臨床表現(xiàn)復雜,，有急性敗血癥者常伴多處化膿性損害,，慢性者類似空洞型肺結核表現(xiàn)。病情一般較為嚴重,，如不及時治療,，病死率甚高。（生物谷Bioon.com)
doi:10.1126/science.1211915
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A Burkholderia pseudomallei Toxin Inhibits Helicase Activity of Translation Factor eIF4A
Cécile Crosnier,Leyla Y. Bustamante,S. Josefin Bartholdson,Amy K. Bei,Michel Theron,Makoto Uchikawa,Souleymane Mboup,Omar Ndir,Dominic P. Kwiatkowski,Manoj T. Duraisingh,Julian C. Rayner& Gavin J. Wrightet al.
Erythrocyte invasion by Plasmodium falciparum is central to the pathogenesis of malaria. Invasion requires a series of extracellular recognition events between erythrocyte receptors and ligands on the merozoite, the invasive form of the parasite. None of the few known receptor–ligand interactions involved are required in all parasite strains, indicating that the parasite is able to access multiple redundant invasion pathways. Here, we show that we have identified a receptor–ligand pair that is essential for erythrocyte invasion in all tested P. falciparum strains. By systematically screening a library of erythrocyte proteins, we have found that the Ok blood group antigen, basigin, is a receptor for PfRh5, a parasite ligand that is essential for blood stage growth. Erythrocyte invasion was potently inhibited by soluble basigin or by basigin knockdown, and invasion could be completely blocked using low concentrations of anti-basigin antibodies; importantly, these effects were observed across all laboratory-adapted and field strains tested. Furthermore, Oka− erythrocytes, which express a basigin variant that has a weaker binding affinity for PfRh5, had reduced invasion efficiencies. Our discovery of a cross-strain dependency on a single extracellular receptor–ligand pair for erythrocyte invasion by P. falciparum provides a focus for new anti-malarial therapies.
