The bovine herpesvirus 1 gene encoding infected cell protein 0 (bICP0) can inhibit interferon-dependent transcription in the absence of other viral genes

Gail Henderson, Yange Zhang, Clinton Jones

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

The infected cell protein 0 (bICP0) encoded by Bovine herpesvirus 1 (BHV-1) stimulates viral gene expression and productive infection. As bICP0 is expressed constitutively during productive infection, it is considered to be the major viral regulatory protein. Like other alphaherpesvirus ICP0 homologues, bICP0 contains a zinc RING finger near its N terminus that activates transcription and regulates subcellular localization. In this study, evidence is provided that bICP0 represses the human beta interferon (IFN-β) promoter and a simple promoter with consensus IFN-stimulated response elements following stimulation with double-stranded RNA (polyinosinic-polycytidylic acid), IFN regulatory factor 3 (IRF3) or IRF7. bICP0 also inhibits the ability of two protein kinases (TBK1 and IKKε) to activate IFN-β promoter activity. The zinc RING finger is necessary for inhibiting IFN-dependent transcription in certain cell types. Collectively, these studies suggest that bICP0 activates productive infection by stimulating viral gene expression and inhibiting IFN-dependent transcription.

Original languageEnglish (US)
Pages (from-to)2697-2702
Number of pages6
JournalJournal of General Virology
Volume86
Issue number10
DOIs
StatePublished - Oct 1 2005

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Bovine Herpesvirus 1
Viral Genes
Interferons
Zinc Fingers
Genes
Viral Regulatory and Accessory Proteins
Proteins
Infection
Interferon Regulatory Factor-3
Gene Expression
Poly I-C
Double-Stranded RNA
Interferon-beta
Response Elements
Protein Kinases

ASJC Scopus subject areas

  • Virology

Cite this

The bovine herpesvirus 1 gene encoding infected cell protein 0 (bICP0) can inhibit interferon-dependent transcription in the absence of other viral genes. / Henderson, Gail; Zhang, Yange; Jones, Clinton.

In: Journal of General Virology, Vol. 86, No. 10, 01.10.2005, p. 2697-2702.

Research output: Contribution to journalArticle

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