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

被引:8
|
作者
Pourcelot, Marie [1 ]
Amaral Moraes, Rayane [1 ]
Fablet, Aurore [1 ]
Breard, Emmanuel [1 ]
Sailleau, Corinne [1 ]
Viarouge, Cyril [1 ]
Postic, Lydie [1 ]
Zientara, Stephan [1 ]
Caignard, Gregory [1 ]
Vitour, Damien [1 ]
机构
[1] Univ Paris Est, Ecole Natl Vet Alfort, ANSES, Dept Anim,UMR 1161,Virol,Lab Anim Hlth,INRAE, F-94700 Maisons Alfort, France
来源
VIRUSES-BASEL | 2021年 / 13卷 / 02期
关键词
Bluetongue virus; VP3; MAVS; IKKε type-I interferons; virus– host interactions;
D O I
10.3390/v13020230
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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-alpha/beta]) 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-beta 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 IKK epsilon. Overall, this study describes a putative role for the BTV structural protein VP3 in the control of the antiviral response.
引用
收藏
页数:10
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