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TRIM29 promotes DNA virus infections by inhibiting innate immune response

Author

Listed:
  • Junji Xing

    (Houston Methodist Research Institute)

  • Ao Zhang

    (Sun Yat-sen University Cancer Center)

  • Hua Zhang

    (Sun Yat-sen University Cancer Center)

  • Jin Wang

    (Houston Methodist Research Institute)

  • Xian Chang Li

    (Houston Methodist Research Institute
    Weill Cornell Medical College of Cornell University)

  • Mu-Sheng Zeng

    (Sun Yat-sen University Cancer Center
    Sun Yat-sen University Cancer Center)

  • Zhiqiang Zhang

    (Houston Methodist Research Institute
    Weill Cornell Medical College of Cornell University)

Abstract

Many double-stranded DNA viruses, such as Epstein-Barr virus, can establish persistent infection, but the underlying virus–host interactions remain poorly understood. Here we report that in human airway epithelial cells Epstein-Barr virus induces TRIM29, a member of the TRIM family of proteins, to inhibit innate immune activation. Knockdown of TRIM29 in airway epithelial cells enhances type I interferon production, and in human nasopharyngeal carcinoma cells results in almost complete Epstein-Barr virus clearance. TRIM29 is also highly induced by cytosolic double-stranded DNA in myeloid dendritic cells. TRIM29 −/− mice have lower adenovirus titers in the lung, and are resistant to lethal herpes simplex virus-1 infection due to enhanced production of type I interferon. Mechanistically, TRIM29 induces K48-linked ubiquitination of Stimulator of interferon genes, a key adaptor in double-stranded DNA-sensing pathway, followed by its rapid degradation. These data demonstrate that Epstein-Barr virus and possible other double-stranded DNA viruses use TRIM29 to suppress local innate immunity, leading to the persistence of DNA virus infections.

Suggested Citation

  • Junji Xing & Ao Zhang & Hua Zhang & Jin Wang & Xian Chang Li & Mu-Sheng Zeng & Zhiqiang Zhang, 2017. "TRIM29 promotes DNA virus infections by inhibiting innate immune response," Nature Communications, Nature, vol. 8(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00101-w
    DOI: 10.1038/s41467-017-00101-w
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    Cited by:

    1. Grant Broussard & Guoxin Ni & Zhigang Zhang & Qian Li & Patricio Cano & Dirk P. Dittmer & Blossom Damania, 2023. "Barrier-to-autointegration factor 1 promotes gammaherpesvirus reactivation from latency," Nature Communications, Nature, vol. 14(1), pages 1-14, December.
    2. Junying Wang & Wenting Lu & Jerry Zhang & Yong Du & Mingli Fang & Ao Zhang & Gabriel Sungcad & Samantha Chon & Junji Xing, 2024. "Loss of TRIM29 mitigates viral myocarditis by attenuating PERK-driven ER stress response in male mice," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    3. Zhibin Lin & Peijun Yang & Yufeng Hu & Hao Xu & Juanli Duan & Fei He & Kefeng Dou & Lin Wang, 2023. "RING finger protein 13 protects against nonalcoholic steatohepatitis by targeting STING-relayed signaling pathways," Nature Communications, Nature, vol. 14(1), pages 1-19, December.

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