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干扰素诱导的GTP酶mGBP-2对水疱性口炎病毒(VSV)和脑心肌炎病毒(EMCV)复制的抑制作用:对野生型GTP结合结构域的不同需求

Inhibition of VSV and EMCV replication by the interferon-induced GTPase, mGBP-2: differential requirement for wild-type GTP binding domain.

作者信息

Carter C C, Gorbacheva V Y, Vestal D J

机构信息

Department of Biological Sciences, University of Toledo, Toledo, Ohio 43606, USA.

出版信息

Arch Virol. 2005 Jun;150(6):1213-20. doi: 10.1007/s00705-004-0489-2. Epub 2005 Feb 18.

Abstract

Interferons (IFNs) exert their anti-viral activities through the induction of anti-viral proteins. One member of the guanylate binding protein (GBP) family of IFN-induced GTPases, hGBP-1, has previously been shown to contribute to the antiviral activities of IFNs. Murine GBP-2 inhibited the replication of both vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV). A wild type GTP binding motif was not required for VSV inhibition but was required for inhibition of EMCV. This is the first demonstration of the role of enzymatic activity in the antiviral activities of GBPs and these findings suggest different mechanisms of inhibition for the two viruses.

摘要

干扰素(IFNs)通过诱导抗病毒蛋白发挥其抗病毒活性。IFN诱导的GTP酶鸟苷酸结合蛋白(GBP)家族的一个成员hGBP-1,先前已被证明有助于IFNs的抗病毒活性。小鼠GBP-2抑制水疱性口炎病毒(VSV)和脑心肌炎病毒(EMCV)的复制。VSV抑制不需要野生型GTP结合基序,但EMCV抑制需要。这是首次证明酶活性在GBPs抗病毒活性中的作用,这些发现提示了两种病毒不同的抑制机制。

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