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The structural basis of herpesvirus entry
Nature Reviews Microbiology ( IF 88.1 ) Pub Date : 2020-10-21 , DOI: 10.1038/s41579-020-00448-w
Sarah A Connolly 1 , Theodore S Jardetzky 2 , Richard Longnecker 3
Affiliation  

Herpesviruses are ubiquitous, double-stranded DNA, enveloped viruses that establish lifelong infections and cause a range of diseases. Entry into host cells requires binding of the virus to specific receptors, followed by the coordinated action of multiple viral entry glycoproteins to trigger membrane fusion. Although the core fusion machinery is conserved for all herpesviruses, each species uses distinct receptors and receptor-binding glycoproteins. Structural studies of the prototypical herpesviruses herpes simplex virus 1 (HSV-1), HSV-2, human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) entry glycoproteins have defined the interaction sites for glycoprotein complexes and receptors, and have revealed conformational changes that occur on receptor binding. Recent crystallography and electron microscopy studies have refined our model of herpesvirus entry into cells, clarifying both the conserved features and the unique features. In this Review, we discuss recent insights into herpesvirus entry by analysing the structures of entry glycoproteins, including the diverse receptor-binding glycoproteins (HSV-1 glycoprotein D (gD), EBV glycoprotein 42 (gp42) and HCMV gH–gL–gO trimer and gH–gL–UL128–UL130–UL131A pentamer), as well gH–gL and the fusion protein gB, which are conserved in all herpesviruses.



中文翻译:

疱疹病毒进入的结构基础

疱疹病毒是无处不在的双链 DNA 包膜病毒,可导致终生感染并引起一系列疾病。进入宿主细胞需要病毒与特定受体结合,然后多种病毒进入糖蛋白的协同作用触发膜融合。尽管所有疱疹病毒的核心融合机制都是保守的,但每个物种都使用不同的受体和受体结合糖蛋白。原型疱疹病毒单纯疱疹病毒 1 (HSV-1)、HSV-2、人类巨细胞病毒 (HCMV) 和爱泼斯坦-巴尔病毒 (EBV) 进入糖蛋白的结构研究确定了糖蛋白复合物和受体的相互作用位点,并揭示了构象受体结合时发生的变化。最近的晶体学和电子显微镜研究改进了我们的疱疹病毒进入细胞的模型,阐明了保守特征和独特特征。在这篇综述中,我们通过分析进入糖蛋白的结构,包括多种受体结合糖蛋白(HSV-1 糖蛋白 D (gD)、EBV 糖蛋白 42 (gp42) 和 HCMV gH-gL-gO 三聚体)的结构,讨论了最近对疱疹病毒进入的见解和 gH–gL–UL128–UL130–UL131A 五聚体),以及 gH–gL 和融合蛋白 gB,它们在所有疱疹病毒中都是保守的。

更新日期:2020-10-28
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