regulation of innate immune responses by bovine herpesvirus 1 and infected cell protein 0 (bicp0)先天免疫反应的调节牛疱疹病毒1和感染细胞蛋白质0(bicp0).pdfVIP

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regulation of innate immune responses by bovine herpesvirus 1 and infected cell protein 0 (bicp0)先天免疫反应的调节牛疱疹病毒1和感染细胞蛋白质0(bicp0).pdf

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regulation of innate immune responses by bovine herpesvirus 1 and infected cell protein 0 (bicp0)先天免疫反应的调节牛疱疹病毒1和感染细胞蛋白质0(bicp0)

Viruses 2009, 1, 255-275; doi:10.3390/v1020255 OPEN ACCESS viruses ISSN 1999-4915 /journal/viruses Review Regulation of Innate Immune Responses by Bovine Herpesvirus 1 and Infected Cell Protein 0 (bICP0) Clinton Jones Department of Veterinary and Biomedical Sciences, Nebraska Center for Virology, University of Nebraska, Lincoln, Fair Street at East Campus Loop, Lincoln, NE, 68583-0905, USA; E-mail: cjones@; Tel.: +1 (402) 472-1890; Fax: +1 (402) 472-9690 Received: 15 July 2009; in revised form: 24 August 2009 / Accepted: 2 September 2009 / Published: 7 September 2009 Abstract: Bovine herpesvirus 1 (BoHV-1) infected cell protein 0 (bICP0) is an important transcriptional regulatory protein that stimulates productive infection. In transient transfection assays, bICP0 also inhibits interferon dependent transcription. bICP0 can induce degradation of interferon stimulatory factor 3 (IRF3), a cellular transcription factor that is crucial for activating beta interferon (IFN-) promoter activity. Recent studies also concluded that interactions between bICP0 and IRF7 inhibit trans-activation of IFN- promoter activity. The C3HC4 zinc RING (really important new gene) finger located near the amino terminus of bICP0 is important for all known functions of bICP0. A recombinant virus that contains a single amino acid change in a well conserved cysteine residue of the C3HC4 zinc RING finger of bICP0 grows poorly in cultured cells, and does not reactivate from latency in cattl