Carbohydrate-binding molecules inhibit viral fusion and entry by crosslinking membrane glycoproteins
Carbohydrate-binding molecules inhibit viral fusion and entry by crosslinking membrane glycoproteins
复制标题
DOI：
10.1038/ni1248
复制
发表时间：
2005-10-01
影响因子：
30.5
通讯作者：
Chernomordik, LV
中科院分区：
文献类型：
--
作者：
Leikina, E;Delanoe-Ayari, H;Chernomordik, LV
防御素是保护宿主免受微生物侵害的肽。在这里，我们表明，θ-防御素逆转录细胞周期蛋白2（RC 2）抑制流感病毒的感染，通过阻断膜融合介导的病毒血凝素。RC 2是有效的，即使在血凝素达到融合构象或诱导膜半融合。RC 2是一种多价凝集素，通过建立交联和固定化表面糖蛋白的网络来阻止血凝素介导的融合。RC 2还抑制辛德毕斯病毒和杆状病毒介导的融合。人类β-防御素3和甘露聚糖结合凝集素也通过产生固定化表面蛋白的保护屏障来阻断病毒融合。这种一般机制可以解释许多先天免疫系统的多价凝集素的广谱抗病毒活性。
Defensins are peptides that protect the host against microorganisms. Here we show that the theta-defensin retrocyclin 2 (RC2) inhibited influenza virus infection by blocking membrane fusion mediated by the viral hemagglutinin. RC2 was effective even after hemagglutinin attained a fusogenic conformation or had induced membrane hemifusion. RC2, a multivalent lectin, prevented hemagglutinin-mediated fusion by erecting a network of crosslinked and immobilized surface glycoproteins. RC2 also inhibited fusion mediated by Sindbis virus and baculovirus. Human beta-defensin 3 and mannan-binding lectin also blocked viral fusion by creating a protective barricade of immobilized surface proteins. This general mechanism might explain the broad-spectrum antiviral activity of many multivalent lectins of the innate immune system.