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

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.

Authors:
;  [1]
  1. Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Avenue, Boston 02115 (United States)
Publication Date:
OSTI Identifier:
21140986
Resource Type:
Journal Article
Journal Name:
Virology
Additional Journal Information:
Journal Volume: 374; Journal Issue: 2; Other Information: DOI: 10.1016/j.virol.2008.01.001; PII: S0042-6822(08)00009-3; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0042-6822
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; GENES; HERPES SIMPLEX; INHIBITION; INTERFERON; PHOSPHORYLATION; VIRUSES

Citation Formats

Johnson, Karen E, Song, Byeongwoon, and Knipe, David M. Role for herpes simplex virus 1 ICP27 in the inhibition of type I interferon signaling. United States: N. p., 2008. Web. doi:10.1016/j.virol.2008.01.001.
Johnson, Karen E, Song, Byeongwoon, & Knipe, David M. Role for herpes simplex virus 1 ICP27 in the inhibition of type I interferon signaling. United States. https://doi.org/10.1016/j.virol.2008.01.001
Johnson, Karen E, Song, Byeongwoon, and Knipe, David M. 2008. "Role for herpes simplex virus 1 ICP27 in the inhibition of type I interferon signaling". United States. https://doi.org/10.1016/j.virol.2008.01.001.
@article{osti_21140986,
title = {Role for herpes simplex virus 1 ICP27 in the inhibition of type I interferon signaling},
author = {Johnson, Karen E and Song, Byeongwoon and Knipe, David M.},
abstractNote = {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.},
doi = {10.1016/j.virol.2008.01.001},
url = {https://www.osti.gov/biblio/21140986}, journal = {Virology},
issn = {0042-6822},
number = 2,
volume = 374,
place = {United States},
year = {Sat May 10 00:00:00 EDT 2008},
month = {Sat May 10 00:00:00 EDT 2008}
}