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本文引用的文献

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Viral and cellular contributions to herpes simplex virus entry into the cell.病毒和细胞因素对单纯疱疹病毒进入细胞的贡献。
Curr Opin Virol. 2012 Feb;2(1):28-36. doi: 10.1016/j.coviro.2011.12.001. Epub 2012 Jan 4.
2
Adherens junction protein nectin-4 is the epithelial receptor for measles virus.粘着连接蛋白 nectin-4 是麻疹病毒的上皮细胞受体。
Nature. 2011 Nov 2;480(7378):530-3. doi: 10.1038/nature10639.
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Structure of herpes simplex virus glycoprotein D bound to the human receptor nectin-1.单纯疱疹病毒糖蛋白 D 与人受体 nectin-1 结合的结构。
PLoS Pathog. 2011 Sep;7(9):e1002277. doi: 10.1371/journal.ppat.1002277. Epub 2011 Sep 29.
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Tumor cell marker PVRL4 (nectin 4) is an epithelial cell receptor for measles virus.肿瘤细胞标志物 PVRL4(神经节苷脂 4)是麻疹病毒的上皮细胞受体。
PLoS Pathog. 2011 Aug;7(8):e1002240. doi: 10.1371/journal.ppat.1002240. Epub 2011 Aug 25.
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Cancer: Tumour-fighting virus homes in.癌症:抗击肿瘤的病毒精准定位。
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Structure of the Newcastle disease virus hemagglutinin-neuraminidase (HN) ectodomain reveals a four-helix bundle stalk.新城疫病毒血凝素-神经氨酸酶(HN)外域结构揭示了一个四螺旋束柄。
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Envelope-chimeric entry-targeted measles virus escapes neutralization and achieves oncolysis.包膜嵌合型入靶麻疹病毒逃避中和作用并实现肿瘤溶解。
Mol Ther. 2011 Oct;19(10):1813-20. doi: 10.1038/mt.2011.92. Epub 2011 May 24.
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Modes of paramyxovirus fusion: a Henipavirus perspective.副黏病毒融合模式:亨德拉尼帕病毒视角。
Trends Microbiol. 2011 Aug;19(8):389-99. doi: 10.1016/j.tim.2011.03.005. Epub 2011 Apr 20.
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Fusing structure and function: a structural view of the herpesvirus entry machinery.融合结构与功能:疱疹病毒进入机制的结构观
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Early target cells of measles virus after aerosol infection of non-human primates.麻疹病毒气溶胶感染非人灵长类动物后的早期靶细胞。
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包膜病毒的靶向进入:麻疹病毒和单纯疱疹病毒 I。

Targeted entry of enveloped viruses: measles and herpes simplex virus I.

机构信息

Department of Molecular Medicine, Virology and Gene Therapy Track, Mayo Graduate School, Rochester, MN 55905, USA.

出版信息

Curr Opin Virol. 2012 Feb;2(1):43-9. doi: 10.1016/j.coviro.2011.12.002. Epub 2011 Dec 23.

DOI:10.1016/j.coviro.2011.12.002
PMID:22440965
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3311990/
Abstract

We compare the receptor-based mechanisms that a small RNA virus and a larger DNA virus have evolved to drive the fusion of viral and cellular membranes. Both systems rely on tight control over triggering the concerted refolding of a trimeric fusion protein. While measles virus entry depends on a receptor-binding protein and a fusion protein only, the herpes simplex virus (HSV) is more complex and requires four viral proteins. Nevertheless, in both viruses a receptor-binding protein is required for triggering the membrane fusion process. Moreover, specificity domains can be appended to these receptor-binding proteins to target virus entry to cells expressing a designated receptor. We discuss how principles established with measles and HSV can be applied to targeting other enveloped viruses, and alternatively how retargeted envelopes can be fitted on foreign capsids.

摘要

我们比较了一种小型 RNA 病毒和一种较大的 DNA 病毒进化出的受体基机制,以驱动病毒和细胞膜融合。这两个系统都依赖于严格控制三聚体融合蛋白的协同重折叠来触发融合。虽然麻疹病毒的进入依赖于受体结合蛋白和融合蛋白,但单纯疱疹病毒 (HSV) 更为复杂,需要四种病毒蛋白。然而,在这两种病毒中,受体结合蛋白都需要触发膜融合过程。此外,可以在这些受体结合蛋白上添加特异性结构域,将病毒进入靶向表达指定受体的细胞。我们讨论了如何将麻疹病毒和 HSV 确立的原则应用于靶向其他包膜病毒,或者如何将重新靶向的包膜适配于外来衣壳。