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Virology. 2008 May 10;374(2):487-94. doi: 10.1016/j.virol.2008.01.001. Epub 2008 Feb 14.

Role for herpes simplex virus 1 ICP27 in the inhibition of type I interferon signaling.

Author information

1
Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Avenue, Boston 02115, USA.

Abstract

Host cells respond to viral infection by many mechanisms, including the production of type I interferons which act in a paracrine and autocrine manner to induce the expression of antiviral interferon-stimulated genes (ISGs). Viruses have evolved means to inhibit interferon signaling to avoid induction of the innate immune response. Herpes simplex virus 1 (HSV-1) has several mechanisms to inhibit type I interferon production, the activities of ISGs, and the interferon signaling pathway itself. We report that the inhibition of the Jak/STAT pathway by HSV-1 requires viral gene expression and that viral immediate-early protein ICP27 plays a role in downregulating STAT-1 phosphorylation and in preventing the accumulation of STAT-1 in the nucleus. We also show that expression of ICP27 by transfection causes an inhibition of IFN-induced STAT-1 nuclear accumulation. Therefore, ICP27 is necessary and sufficient for at least some of the effects of HSV infection on STAT-1.

PMID:
18279905
PMCID:
PMC2638114
DOI:
10.1016/j.virol.2008.01.001
[Indexed for MEDLINE]
Free PMC Article

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