Herpes simplex virus ICP0 and ICP34.5 counteract distinct interferon-induced barriers to virus replication
Herpes simplex virus ICP0 and ICP34.5 counteract distinct interferon-induced barriers to virus replication
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DOI：
10.1128/jvi.76.4.1995-1998.2002
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发表时间：
2002-02-01
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;Smiley, JR
干扰素通过多种机制抑制病毒复制。在这里，我们表明，单纯疱疹病毒蛋白ICP0和ICP34.5克服干扰素诱导的病毒转录和翻译的障碍，分别。这些干扰素诱导的抗病毒机制在已建立的细胞系中差异表达：U2OS细胞不具备ICP0靶向的IFN诱导机制，而Vero细胞可能缺乏ICP34.5靶向的机制。
Interferon inhibits virus replication through multiple mechanisms. Here we show that herpes simplex virus proteins ICP0 and ICP34.5 overcome interferon-induced barriers to viral transcription and translation, respectively. These cytokine-induced antiviral mechanisms are differentially expressed in established cell lines: U2OS cells do not mount the IFN-induced mechanism targeted by ICP0, and Vero cells may be defective for the mechanism targeted by ICP34.5.