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

Journal Article · Sat May 10 04:00:00 EDT 2008 · Virology

DOI:https://doi.org/10.1016/j.virol.2008.01.001· OSTI ID:21140986

Johnson, Karen E; Song, Byeongwoon ^[1]

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1. Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Avenue, Boston 02115 (United States)

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.

• OSTI ID: 21140986
• Journal Information: Virology, Journal Name: Virology Journal Issue: 2 Vol. 374; ISSN VIRLAX; ISSN 0042-6822
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
GENES
HERPES SIMPLEX
INHIBITION
INTERFERON
PHOSPHORYLATION
VIRUSES