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The Capsid Protein of Nervous Necrosis Virus Antagonizes Host Type I IFN Production by a Dual Strategy to Negatively Regulate Retinoic Acid–Inducible Gene-I–like Receptor Pathways

Peng Jia, Wanwan Zhang, Yangxi Xiang, Xiaobing Lu, Xiaoqi Chen, Hongbo Pan, Meisheng Yi and Kuntong Jia
J Immunol July 1, 2022, ji2100690; DOI: https://doi.org/10.4049/jimmunol.2100690
Peng Jia
*Guangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, Pearl River Estuary Marine Ecosystem Research Station, Ministry of Education, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China;
†Fuzhou Medical College of Nanchang University, Fuzhou, Jiangxi, China;
‡Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), Zhuhai, Guangdong, China; and
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Wanwan Zhang
*Guangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, Pearl River Estuary Marine Ecosystem Research Station, Ministry of Education, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China;
‡Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), Zhuhai, Guangdong, China; and
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Yangxi Xiang
*Guangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, Pearl River Estuary Marine Ecosystem Research Station, Ministry of Education, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China;
‡Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), Zhuhai, Guangdong, China; and
§State Key Laboratory for Quality and Safety of Agro-products, Ningbo University, Ningbo, Zhejiang, China
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Xiaobing Lu
*Guangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, Pearl River Estuary Marine Ecosystem Research Station, Ministry of Education, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China;
‡Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), Zhuhai, Guangdong, China; and
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Xiaoqi Chen
*Guangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, Pearl River Estuary Marine Ecosystem Research Station, Ministry of Education, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China;
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Hongbo Pan
*Guangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, Pearl River Estuary Marine Ecosystem Research Station, Ministry of Education, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China;
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Meisheng Yi
*Guangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, Pearl River Estuary Marine Ecosystem Research Station, Ministry of Education, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China;
‡Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), Zhuhai, Guangdong, China; and
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Kuntong Jia
*Guangdong Provincial Key Laboratory of Marine Resources and Coastal Engineering, Pearl River Estuary Marine Ecosystem Research Station, Ministry of Education, School of Marine Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China;
‡Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), Zhuhai, Guangdong, China; and
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Key Points

  • CP potentiates RGNNV proliferation by suppressing the RLR-IFN signaling pathway.

  • CP promotes LjRNF114-mediated K48 ubiquitination and degradation of LjTRAF3.

  • CP promotes the K48-linked ubiquitination and degradation of LjIRF3.

Abstract

Nervous necrosis virus (NNV), a highly pathogenic RNA virus, is a major pathogen in the global aquaculture industry. To efficiently infect fish, NNV must evade or subvert the host IFN for their replication; however, the precise mechanisms remain to be elucidated. In this study, we reported that capsid protein (CP) of red-spotted grouper NNV (RGNNV) suppressed the IFN antiviral response to promote RGNNV replication in Lateolabrax japonicus brain cells, which depended on the ARM, S, and P domains of CP. CP showed an indirect or direct association with the key components of retinoic acid–inducible gene-I–like receptors signaling, L. japonicus TNFR-associated factor 3 (LjTRAF3) and IFN regulatory factor (LjIRF3), respectively, and degraded LjTRAF3 and LjIRF3 through the ubiquitin-proteasome pathway in HEK293T cells. Furthermore, we found that CP potentiated LjTRAF3 K48 ubiquitination degradation in a L. japonicus ring finger protein 114–dependent manner. LjIRF3 interacted with CP through the S domain of CP and the transcriptional activation domain or regulatory domain of LjIRF3. CP promoted LjIRF3 K48 ubiquitination degradation, leading to the reduced phosphorylation level and nuclear translocation of LjIRF3. Taken together, we demonstrated that CP inhibited type I IFN response by a dual strategy to potentiate the ubiquitination degradation of LjTRAF3 and LjIRF3. This study reveals a novel mechanism of RGNNV evading host immune response via its CP protein that will provide insights into the complex pathogenesis of NNV.

Footnotes

  • This work was supported by the National Natural Science Foundation of China (NSF), the Foundation for Innovative Research Groups of the NSF (32173001); the Bureau of Science and Information Technology of Guangzhou Municipality (Pearl River S&T Nova Program of Guangzhou) (201806010047); the China Postdoctoral Science Foundation–Funded Project (2019M653152); the Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) (2019A1515110842); and the Natural Science Foundation of Guangxi Province (Guangxi Natural Science Foundation) (2021GXNSFDA075015).

  • The online version of this article contains supplemental material.

  • Received July 13, 2021.
  • Accepted January 10, 2022.
  • Copyright © 2022 by The American Association of Immunologists, Inc.

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The Journal of Immunology: 209 (4)
The Journal of Immunology
Vol. 209, Issue 4
15 Aug 2022
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The Capsid Protein of Nervous Necrosis Virus Antagonizes Host Type I IFN Production by a Dual Strategy to Negatively Regulate Retinoic Acid–Inducible Gene-I–like Receptor Pathways
Peng Jia, Wanwan Zhang, Yangxi Xiang, Xiaobing Lu, Xiaoqi Chen, Hongbo Pan, Meisheng Yi, Kuntong Jia
The Journal of Immunology July 1, 2022, ji2100690; DOI: 10.4049/jimmunol.2100690

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The Capsid Protein of Nervous Necrosis Virus Antagonizes Host Type I IFN Production by a Dual Strategy to Negatively Regulate Retinoic Acid–Inducible Gene-I–like Receptor Pathways
Peng Jia, Wanwan Zhang, Yangxi Xiang, Xiaobing Lu, Xiaoqi Chen, Hongbo Pan, Meisheng Yi, Kuntong Jia
The Journal of Immunology July 1, 2022, ji2100690; DOI: 10.4049/jimmunol.2100690
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