The VP3 Protein of Bluetongue Virus Associates with the MAVS Complex and Interferes with the RIG-I-Signaling Pathway
2021
Marie Pourcelot | Rayane Amaral Moraes | Aurore Fablet | Emmanuel Bréard | Corinne Sailleau | Cyril Viarouge | Lydie Postic | Stéphan Zientara | Grégory Caignard | Damien Vitour
Bluetongue virus (BTV), an arbovirus transmitted by <i>Culicoides</i> 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.
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