類鼻疽又被稱為“越南定時(shí)”，這種疾病在越南戰(zhàn)爭后引起了人們的極大關(guān)注。隨著美軍直升機(jī)在這個(gè)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(huì)演變出嚴(yán)重的敗血癥，在一些地區(qū)，這種疾病的死亡率甚至高達(dá)40%。

為了找到其中的原因，英國謝菲爾德大學(xué)的分子生物學(xué)家Stuart Wilson和同事對類鼻疽桿菌的一種蛋白質(zhì)BPSL1549進(jìn)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(zhì)是一種細(xì)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(nèi)注射了攜帶BPSL1549及沒有攜帶這種蛋白質(zhì)的類鼻疽桿菌。結(jié)果顯示，前者殺死的嚙齒動(dòng)物數(shù)量是后者的100倍。Wilson說，可見，雖然這種微生物也會(huì)產(chǎn)生其他一些毒素，但BPSL1549無疑是其中*毒的。

研究人員在*新出版的美國《科學(xué)》雜志上報(bào)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(jīng)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(fù)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(jié)核表現(xiàn)。病情一般較為嚴(yán)重，如不及時(shí)治療，病死率甚高。

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, Ok^a− 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