Abstract
Bluetongue virus (BTV), an arbovirus transmitted by Culicoides biting midges, is a major concern of wild and domestic ruminants. While BTV induces type I interferon (alpha/beta interferon [IFN-α/β]) production in infected cells, several reports have described evasion strategies elaborated by this virus to dampen this intrinsic, innate response. In the present study, we suggest that BTV VP3 is a new viral antagonist of the IFN-β synthesis. Indeed, using split luciferase and coprecipitation assays, we report an interaction between VP3 and both the mitochondrial adapter protein MAVS and the IRF3-kinase IKKε. Overall, this study describes a putative role for the BTV structural protein VP3 in the control of the antiviral response.
Keywords:
Bluetongue virus; IKKε; MAVS; VP3; type-I interferons; virus–host interactions.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / metabolism*
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Bluetongue / genetics
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Bluetongue / metabolism*
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Bluetongue / virology
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Bluetongue virus / genetics
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Bluetongue virus / metabolism*
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DEAD Box Protein 58 / genetics
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DEAD Box Protein 58 / metabolism*
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HeLa Cells
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Host-Pathogen Interactions
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Humans
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Interferon Regulatory Factor-3 / genetics
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Interferon Regulatory Factor-3 / metabolism
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Interferon-beta / genetics
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Interferon-beta / metabolism
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Protein Binding
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Receptors, Immunologic / genetics
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Receptors, Immunologic / metabolism*
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Signal Transduction
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Viral Core Proteins / genetics
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Viral Core Proteins / metabolism*
Substances
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Adaptor Proteins, Signal Transducing
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IRF3 protein, human
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Interferon Regulatory Factor-3
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MAVS protein, human
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Receptors, Immunologic
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VP3 protein, Bluetongue virus
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Viral Core Proteins
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Interferon-beta
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RIGI protein, human
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DEAD Box Protein 58