Herpes simplex virus triggers and then disarms a host antiviral response
Herpes simplex virus triggers and then disarms a host antiviral response
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DOI：
10.1128/jvi.75.2.750-758.2001
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发表时间：
2001-01-01
影响因子：
5.4
通讯作者：
Smiley, JR
中科院分区：
文献类型：
--
作者：
Mossman, KL;Macgregor, PF;Smiley, JR
病毒感染诱导主要与可溶性干扰素的合成和分泌相关的抗病毒应答。在这里，我们报告说，单纯疱疹病毒1型病毒粒子诱导干扰素非依赖性抗病毒状态的人胚肺细胞，防止各种病毒的斑块。对19，000个人类表达序列标签的微阵列分析揭示了一组有限的宿主基因的诱导，其中大多数也被干扰素诱导。参与控制病毒细胞内传播和消除病毒感染细胞的基因是被诱导的基因之一。细胞反应的诱导发生在没有从头细胞蛋白质合成的情况下，并且需要病毒渗透。此外，这种反应仅在病毒基因表达被抑制时观察到，这表明新合成的病毒蛋白可能作为这种反应的抑制剂。
Virus infection induces an antiviral response that is predominantly associated with the synthesis and secretion of soluble interferon. Here, we report that herpes simplex virus type 1 virions induce an interferon-independent antiviral state in human embryonic lung cells that prevents plaquing of a variety of viruses. Microarray analysis of 19,000 human expressed sequence tags revealed induction of a limited set of host genes, the majority of which are also induced by interferon. Genes implicated in controlling the intracellular spread of virus and eliminating virally infected cells were among those induced. Induction of the cellular response occurred in the absence of de novo cellular protein synthesis and required viral penetration. In addition, this response was only seen when viral gene expression was inhibited, suggesting that a newly synthesized viral protein(s) may function as an inhibitor of this response.