The VP3 Protein of Bluetongue Virus Associates with the MAVS Complex and Interferes with the RIG-I-Signaling Pathway

蓝舌病病毒的 VP3 蛋白与 MAVS 复合物结合并干扰 RIG-I 信号通路

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作者:Marie Pourcelot, Rayane Amaral Moraes, Aurore Fablet, Emmanuel Bréard, Corinne Sailleau, Cyril Viarouge, Lydie Postic, Stéphan Zientara, Grégory Caignard, Damien Vitour

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.

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