2. Academic Validation
  3. Newcastle disease virus nucleocapsid protein mediates the degradation of 14-3-3ε to antagonize the interferon response and promote viral replication

Newcastle disease virus nucleocapsid protein mediates the degradation of 14-3-3ε to antagonize the interferon response and promote viral replication

  • Vet Microbiol. 2023 Aug 15;284:109851. doi: 10.1016/j.vetmic.2023.109851.
Qiufan Xu 1,  Jianpeng Liang 2,  Jiaqi Jin 1,  Wanyan Wu 1,  Jinlian Ren 1,  Jiayu Ruan 1,  Lei Fan 1,  Weifeng Yuan 1,  Juncheng Cai 1,  Qiuyan Lin 1,  Bin Xiang 3,  Chan Ding 4,  Tao Ren 1,  Libin Chen 5
Affiliations

Affiliations

  • 1 College of Veterinary Medicine, South China Agricultural University, Guangzhou, China; Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, China; National and Regional Joint Engineering Laboratory for Medicament of Zoonosis Prevention and Control, Guangzhou, China; Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, Guangzhou, China.
  • 2 Moganshan Institute Zhejiang University of Technology, Hangzhou, Zhejiang, China.
  • 3 College of Veterinary Medicine, Yunnan Agricultural University, Kunming, Yunnan, China.
  • 4 Shanghai Veterinary Research Institute (SHVRI), Chinese Academy of Agricultural Sciences (CAAS), Shanghai, China.
  • 5 College of Veterinary Medicine, South China Agricultural University, Guangzhou, China; Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, China; National and Regional Joint Engineering Laboratory for Medicament of Zoonosis Prevention and Control, Guangzhou, China; Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, Guangzhou, China. Electronic address: chenlibin@scau.edu.cn.
PMID: 37598526 DOI: 10.1016/j.vetmic.2023.109851
Abstract

Newcastle disease virus (NDV) is responsible for outbreaks that pose a threat to the global poultry industry. NDV triggers an interferon (IFN) response in the host upon Infection. However, it also employs mechanisms that counteract this response. One important component in IFN-related signaling pathways is 14-3-3ε, which is known to interact with retinoic acid-inducible gene I (RIG-I) and mitochondrial Antiviral signaling protein (MAVS). The relationship between 14 and 3-3ε and NDV Infection has not been previously explored; therefore, this study aimed to investigate this relationship in vivo and in vitro using overexpressed and knockdown 14-3-3ε experiments, along with co-immunoprecipitation analysis. We found that NDV Infection led to the degradation of 14-3-3ε. Furthermore, 14-3-3ε inhibited the replication of NDV, suggesting that NDV may enhance its own replication by promoting the degradation of 14-3-3ε during Infection. The study revealed that 14-3-3ε is degraded by lysosomes and the viral protein nucleocapsid protein (NP) of NDV induces this degradation. It was also observed that 14-3-3ε is involved in activating the IFN pathway during NDV Infection and mediates the binding of MDA5 to MAVS. Our study reveals that NDV NP mediates the entry of 14-3-3ε into lysosomes and facilitates its degradation. These findings contribute to the existing knowledge on the molecular mechanisms employed by NDV to counteract the IFN response and enhance its own replication.

Keywords

14–3–3ε; Interferon response; Newcastle disease virus; Nucleocapsid protein; Viral replication.

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