Abstract
The bICP0 protein encoded by bovine herpesvirus 1 stimulates productive infection and viral gene expression but inhibits interferon (IFN)-dependent transcription. bICP0 inhibits beta IFN (IFN-beta) promoter activity and induces degradation of IFN regulatory factor 3 (IRF3). Although bICP0 inhibits the trans-activation activity of IRF7, IRF7 protein levels are not reduced. In this study, we demonstrate that bICP0 is associated with IRF7. Furthermore, bICP0 inhibits the ability of IRF7 to trans-activate the IFN-beta promoter in the absence of IRF3 expression. The interaction between bICP0 and IRF7 correlates with reduced trans-activation of the IFN-beta promoter by IRF7.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Cell Line, Tumor
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Herpesvirus 1, Bovine / immunology*
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Herpesvirus 1, Bovine / physiology
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Interferon Regulatory Factor-3 / metabolism
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Interferon Regulatory Factor-7 / antagonists & inhibitors*
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Interferon Regulatory Factor-7 / metabolism*
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Interferon-beta / biosynthesis*
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Mice
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Promoter Regions, Genetic*
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Protein Binding
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Trans-Activators / metabolism*
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Ubiquitin-Protein Ligases / metabolism*
Substances
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Interferon Regulatory Factor-3
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Interferon Regulatory Factor-7
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Trans-Activators
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Interferon-beta
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Ubiquitin-Protein Ligases
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bICP0 protein, Bovine herpesvirus 1