Herpesvirus Entry into Host Cells Mediated by Endosomal Low pH.
Herpesvirus Entry into Host Cells Mediated by Endosomal Low pH.
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DOI：
10.1111/tra.12408
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发表时间：
2016-09
期刊：
影响因子：
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通讯作者：
Nicola AV
中科院分区：
文献类型：
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作者：
Nicola AV
疱疹病毒的发病机制源于多种细胞类型的感染，包括潜伏位点和支持裂解复制的细胞。疱疹病毒利用不同的细胞途径，包括低pH内吞途径，进入不同的病理生理相关的靶细胞。这篇综述详细介绍了温和的酸性环境内体对疱疹病毒进入的影响，特别强调单纯疱疹病毒1型（HSV-1）。上皮细胞，原发性HSV-1感染的门户，支持通过低pH内吞机制进入。弱酸性pH触发HSV-1 III类融合蛋白糖蛋白B（gB）的可逆构象变化。在体外处理具有相似pH范围的单纯疱疹病毒粒子可灭活感染性，这可能是通过在缺乏靶膜的情况下过早激活病毒进入机制。给定的疱疹病毒如何介导低pH和pH非依赖性进入事件是一个关键的未解决的问题。
Herpesviral pathogenesis stems from infection of multiple cell types including the site of latency and cells that support lytic replication. Herpesviruses utilize distinct cellular pathways, including low pH endocytic pathways, to enter different pathophysiologically relevant target cells. This review details the impact of the mildly acidic mileu of endosomes on the entry of herpesviruses, with particular emphasis on herpes simplex virus 1 (HSV-1). Epithelial cells, the portal of primary HSV-1 infection, support entry via low pH endocytosis mechanisms. Mildly acidic pH triggers reversible conformational changes in the HSV-1 class III fusion protein glycoprotein B (gB). In vitro treatment of herpes simplex virions with a similar pH range inactivates infectivity, likely by prematurely activating the viral entry machinery in the absence of a target membrane. How a given herpesvirus mediates both low pH and pH-independent entry events is a key unresolved question.