Newcastle Disease Virus V Protein Degrades Mitochondrial Antiviral Signaling Protein To Inhibit Host Type I Interferon Production via E3 Ubiquitin Ligase RNF5

Author:

Sun Yingjie1,Zheng Hang2,Yu Shengqing1,Ding Yunlei1,Wu Wei1,Mao Xuming1,Liao Ying1,Meng Chunchun1,Ur Rehman Zaib1,Tan Lei1,Song Cuiping1,Qiu Xusheng1,Wu Fengyun1,Ding Chan13

Affiliation:

1. Department of Avian Infectious Diseases, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, People’s Republic of China

2. College of Animal Science and Technology, Jilin Agricultural University, Changchun, People’s Republic of China

3. Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, People’s Republic of China

Abstract

Host anti-RNA virus innate immunity relies mainly on the recognition by retinoic acid-inducible gene I and melanoma differentiation-associated protein 5 and subsequently initiates downstream signaling through interaction with MAVS. On the other hand, viruses have developed various strategies to counteract MAVS-mediated signaling. The mechanism for paramyxoviruses regulating MAVS to benefit their infection remains unknown. In this article, we demonstrate that the V proteins of NDV and several other paramyxoviruses target MAVS for ubiquitin-mediated degradation through E3 ubiquitin ligase RING-finger protein 5 (RNF5). MAVS degradation leads to the inhibition of the downstream IFN-β pathway and therefore benefits virus proliferation. Our study reveals a novel mechanism of NDV evading host innate immunity and provides insight into the therapeutic strategies for the control of paramyxovirus infection.

Funder

National Key Research and Development Program of China

National Natural Science Foundation of China

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

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