Expression of herpes simplex virus ICP0 inhibits the induction of interferon-stimulated genes by viral infection

被引：141

作者：

Eidson, KM ^{[1
]}

Hobbs, WE ^{[1
]}

Manning, BJ ^{[1
]}

Carlson, P ^{[1
]}

DeLuca, NA ^{[1
]}

机构：

[1] Univ Pittsburgh, Sch Med, Dept Mol Genet & Biochem, Pittsburgh, PA 15261 USA

来源：

JOURNAL OF VIROLOGY | 2002年 / 76卷 / 05期

关键词：

D O I：

10.1128/JVI.76.5.2180-2191.2002

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

The herpes simplex virus type 1 (HSV-1) mutant d109 does not express any of the immediate-early (IE) proteins and persists in cells for a prolonged length of time. As has been shown by Nicholl et al. (J. Gen. Virol. 81:2215-2218, 2000) and Mossman et al. (J. Virol. 75:750-758, 2001) using other mutants defective for IE gene expression, infection with d109 induced the expression of a number of interferon-stimulated genes. Induction of these genes was significantly greater at multiplicities of infection (MOI) of 10 PFU/cell or greater, and the resulting antiviral effect was only seen at MOIs greater than 10 PFU/cell. Using mutants defective for sets of IE genes established that the lack of ICP0 expression was necessary for high levels of interferon-stimulated gene expression in HEL cells. The induction of interferon-stimulated genes by d109 could also be inhibited by infection with an E1-:E3-:E4- adenovirus expressing levels of ICP0 that are comparable to those expressed within the first hour of wild-type virus infection. Lastly, the addition of the proteasome inhibitor MG132 to cells infected with a mutant that expresses ICP0, d106, also resulted in the induction of interferon-stimulated genes. Thus, ICP0 may function through the proteasome very early in HSV infection to inhibit a cellular antiviral response induced by the virion.

引用

页码：2180 / 2191

页数：12

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