Herpes simplex virus type 1 induces filopodia in differentiated P19 neural cells to facilitate viral spread
Herpes simplex virus type 1 induces filopodia in differentiated P19 neural cells to facilitate viral spread
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DOI：
10.1016/j.neulet.2008.05.031
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发表时间：
2008-08-01
影响因子：
2.5
通讯作者：
Shukla, Deepak
中科院分区：
文献类型：
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作者：
Dixit, Rohan;Tiwari, Vaibhav;Shukla, Deepak
单纯疱疹病毒1型(HSV-1)是一种嗜神经性病毒，具有作为中枢神经系统(CNS)基因治疗病毒载体的巨大潜力。这项研究为表达重组绿色荧光蛋白(GFP)的HSV-1沿着分化的P19神经元样细胞的树突向下有效到达胞体提供了直观的证据。该病毒还促进细胞骨架重排，从而促进病毒在体外的传播，包括树突状丝状足突的急剧增加。肌动蛋白聚合抑制剂细胞松弛素D分别减少了病毒移动、细胞感染和丝足诱导，这表明肌动蛋白皮质参与了这些过程。对HSV-I反应中神经细胞骨架重组的观察可能有助于阐明与疱疹病毒性脑炎相关的急性病毒感染导致患者认知障碍的机制。(C)2008爱思唯尔爱尔兰有限公司。保留所有权利。
Herpes simplex virus type-1 (HSV-1) is a neurotropic virus with significant potential as a viral vector for central nervous system (CNS) gene therapy. This study provides visual evidence that recombinant green fluorescent protein (GFP)-expressing HSV-1 travel down dendrites in differentiated P19 neuronal-like cells to efficiently reach the soma. The virus also promotes cytoskeletal rearrangements which facilitate viral spread in vitro, including often dramatic increases in dendritic filopodia. Viral movements, cell infection and filopodia induction were each reduced with the actin polymerization inhibitor cytochalasin D, suggesting the involvement of the actin cortex in these processes. The observation of neural cytoskeletal reorganization in response to HSV-I may shed light on the mechanisms by which acute viral infection associated with herpes encephalitis produces cognitive deficits in patients. (c) 2008 Elsevier Ireland Ltd. All rights reserved.