CoREST 缺失并不能提高 ICP0 缺失突变型单纯疱疹病毒 1 的复制。
Depletion of CoREST does not improve the replication of ICP0 null mutant herpes simplex virus type 1.
机构信息
MRC Virology Unit, Institute of Virology, Church Street, Glasgow G11 5JR, Scotland, United Kingdom.
出版信息
J Virol. 2010 Apr;84(7):3695-8. doi: 10.1128/JVI.00021-10. Epub 2010 Jan 27.
Abstract
It has been proposed that the cellular corepressor protein CoREST is involved in repressing herpes simplex virus type 1 (HSV-1) infection in the absence of the viral regulatory protein ICP0. This proposal predicts that depletion of CoREST should improve the plaque-forming efficiency and replication of ICP0 null mutant virus. To test this hypothesis, human HepaRG cells that were highly depleted of CoREST were isolated using RNA interference technology. Depletion of CoREST had no effect on the replication of ICP0 null mutant HSV-1, demonstrating that CoREST does not play an influential role in regulating HSV-1 infection in this cell type.
摘要
有人提出，细胞核心抑制蛋白 CoREST 参与在没有病毒调节蛋白 ICP0 的情况下抑制单纯疱疹病毒 1 型（HSV-1）的感染。这一假说预测，CoREST 的耗竭应该会提高 ICP0 缺失突变病毒的噬菌斑形成效率和复制。为了验证这一假设，使用 RNA 干扰技术从 HepaRG 细胞中高度耗竭 CoREST 以分离细胞。CoREST 的耗竭对 ICP0 缺失突变 HSV-1 的复制没有影响，表明 CoREST 在这种细胞类型中对调节 HSV-1 感染不起重要作用。
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7
STAT-1- and IRF-3-dependent pathways are not essential for repression of ICP0-null mutant herpes simplex virus type 1 in human fibroblasts.STAT-1和IRF-3依赖的信号通路对于人成纤维细胞中ICP0缺失突变的单纯疱疹病毒1型的抑制并非必需。
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