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卡波氏肉瘤相关疱疹病毒病毒干扰素调节因子-2 通过靶向干扰素刺激基因因子-3 抑制 I 型干扰素信号转导。

Kaposi's sarcoma-associated herpesvirus viral interferon regulatory factor-2 inhibits type 1 interferon signalling by targeting interferon-stimulated gene factor-3.

机构信息

School of Cancer Sciences and Cancer Research UK Cancer Centre, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK.

School of Clinical and Experimental Medicine, College of Medical & Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK.

出版信息

J Gen Virol. 2011 Oct;92(Pt 10):2394-2398. doi: 10.1099/vir.0.034322-0. Epub 2011 Jun 22.

DOI:10.1099/vir.0.034322-0
PMID:21697347
Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) encodes four viral interferon regulatory factors (vIRF-1-4). We investigated the mechanism and consequences of vIRF-2-mediated inhibition of interferon-response element signalling following type I interferon (IFN) induction. Western blot and electrophoretic mobility-shift assays identified the interferon-stimulated gene factor-3 (ISGF-3) components STAT1 and IRF-9 as the proximal targets of vIRF-2 activity. The biological significance of vIRF-2 inhibition of ISGF-3 was demonstrated by vIRF-2-mediated rescue of the replication of the IFN-sensitive virus encephalomyocarditis virus. This study provides both a mechanism and evidence for KSHV vIRF-2-mediated suppression of the consequences of type 1 IFN-induced signalling.

摘要

卡波济氏肉瘤相关疱疹病毒(KSHV)编码四个病毒干扰素调节因子(vIRF-1-4)。我们研究了 vIRF-2 介导的在 I 型干扰素(IFN)诱导后抑制干扰素反应元件信号的机制和后果。Western blot 和电泳迁移率变动分析鉴定出干扰素刺激基因因子 3(ISGF-3)的成分 STAT1 和 IRF-9 是 vIRF-2 活性的近端靶标。vIRF-2 介导的对 IFN 敏感的病毒脑炎心肌炎病毒复制的挽救证明了 vIRF-2 抑制 ISGF-3 的生物学意义。这项研究提供了 KSHV vIRF-2 介导的抑制 1 型 IFN 诱导信号的后果的机制和证据。

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