Cited by 129interferon and immune responsesImmune Response and InflammationAutophagy in Disease and Therapy

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COX5B Regulates MAVS-mediated Antiviral Signaling through Interaction with ATG5 and Repressing ROS Production

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Zhao, Yuanyuan, Sun, Xiaofeng, Nie, Xuanli, Sun, Liwei, Tang, Tie-shan, Chen, Dahua, Sun, Qinmiao·2012·PLoS Pathogens

DOI 10.1371/journal.ppat.1003086PMC PMC3534373

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Abstract

Innate antiviral immunity is the first line of the host defense system that rapidly detects invading viruses. Mitochondria function as platforms for innate antiviral signal transduction in mammals through the adaptor protein, MAVS. Excessive activation of MAVS-mediated antiviral signaling leads to dysfunction of mitochondria and cell apoptosis that likely causes the pathogenesis of autoimmunity. However, the mechanism of how MAVS is regulated at mitochondria remains unknown. Here we show that the Cytochrome c Oxidase (CcO) complex subunit COX5B physically interacts with MAVS and negatively regulates the MAVS-mediated antiviral pathway. Mechanistically, we find that while activation of MAVS leads to increased ROS production and COX5B expression, COX5B down-regulated MAVS signaling by repressing ROS production. Importantly, our study reveals that COX5B coordinates with the autophagy pathway to control MAVS aggregation, thereby balancing the antiviral signaling activity. Thus, our study provides novel insights into the link between mitochondrial electron transport system and the autophagy pathway in regulating innate antiviral immunity.

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Authors: Zhao, Y., Sun, X., Nie, X., Sun, L., Tang, T.-S., Chen, D., & Sun, Q.
Affiliations: Chinese Academy of Sciences (CN)
Corresponding author: Sun, Qinmiao
ORCID: Zhao, Yuanyuan
Sun, Liwei
Tang, Tie-shan
Chen, Dahua
Sun, Qinmiao
Venue: PLoS Pathogens
Publisher: Public Library of Science (PLoS)
Published: 2012-12-20
Volume: 8
Issue: 12
Pages: e1003086
ISSN: 1553-7366 (ISSN-L)
1553-7374
DOI: 10.1371/journal.ppat.1003086
PMC: PMC3534373
OpenAlex: W1974115318
Cited by: 129
References: 53
Citations by year: 2026: 4 · 2025: 4 · 2024: 11 · 2023: 10 · 2022: 7 · 2021: 11 · 2020: 13 · 2019: 8 · 2018: 11 · 2017: 10 · 2016: 14 · 2015: 14 · 2014: 9 · 2013: 3
FWCI: 3.62
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
Locations: PLoS Pathogens (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: University of Texas Southwestern Medical Center
National Natural Science Foundation of China (2010CB945300)
Chinese Academy of Sciences
Tsinghua University
Wuhan University
National Key Research and Development Program of China (2010CB945300)
Topics: Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords: COX5B, MAVS, cytochrome c oxidase, antiviral signaling, reactive oxygen species, autophagy, ATG5, mitochondria, antiviral innate immunity, autoimmunity
MeSH terms: Autophagy-Related Protein 5, Animals, Autophagy, Cells, Cultured, Electron Transport Complex IV, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Humans, Immunity, Innate, Microtubule-Associated Proteins, Mitochondria, Protein Binding, RNA, Messenger, Vesicular stomatitis Indiana virus, Virion, Blotting, Western, Signal Transduction, NF-kappa B, Apoptosis, Reactive Oxygen Species, Reverse Transcriptase Polymerase Chain Reaction, Immunoprecipitation, Adaptor Proteins, Signal Transducing, Cell Proliferation, Vesicular Stomatitis, Real-Time Polymerase Chain Reaction

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COX5B Regulates MAVS-mediated Antiviral Signaling through Interaction with ATG5 and Repressing ROS Production

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