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Early Events in Herpes Simplex Virus Lifecycle with Implications for an Infection of Lifetime

机译:单纯疱疹病毒生命周期中的早期事件可能会影响生命周期。

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摘要

Affecting a large percentage of human population herpes simplex virus (HSV) types -1 and -2 mainly cause oral, ocular, and genital diseases. Infection begins with viral entry into a host cell, which may be preceded by viral “surfing” along filopodia. Viral glycoproteins then bind to one or more of several cell surface receptors, such as herpesvirus entry mediator (HVEM), nectin-1, 3-O sulfated heparan sulfate (3-OS HS), paired immunoglobulin-like receptor α, and non-muscle myosin-IIA. At least five viral envelope glycoproteins participate in entry and these include gB, gC, gD and gH-gL. Post-entry, these glycoproteins may also facilitate cell-to-cell spread of the virus, which helps in the evasion of physical barriers as well as several components of the innate and adaptive immune responses. The spread may be facilitated by membrane fusion, movement across tight junctions, transfer across neuronal synapses, or the recruitment of actin-containing structures. This review summarizes some of the recent advances in our understanding of HSV entry and cell-to-cell spread.
机译:感染人口的很大一部分-1型和-2型单纯疱疹病毒(HSV)主要导致口腔,眼部和生殖器疾病。感染始于病毒进入宿主细胞,然后可能是病毒沿着丝状伪足“冲浪”。病毒糖蛋白然后结合几种细胞表面受体中的一种或多种,​​例如疱疹病毒进入介体(HVEM),nectin-1、3-O硫酸硫酸乙酰肝素(3-OS HS),成对的免疫球蛋白样受体α和非肌肉肌球蛋白IIA。至少有五种病毒包膜糖蛋白参与进入,其中包括gB,gC,gD和gH-gL。进入后,这些糖蛋白也可能促进病毒在细胞之间的传播,这有助于规避物理屏障以及先天性和适应性免疫反应的某些组成部分。膜融合,跨紧密连接的移动,跨神经突触的转移或含肌动蛋白的结构的募集可促进扩散。这篇综述总结了我们对HSV进入和细胞间扩散的最新进展。

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