TRIM29 promotes DNA virus infections by inhibiting innate immune response

Junji Xing, Ao Zhang, Hua Zhang, Jin Wang, Xian Chang Li (), Mu-Sheng Zeng () and Zhiqiang Zhang ()
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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
Mu-Sheng Zeng: Sun Yat-sen University Cancer Center
Zhiqiang Zhang: Houston Methodist Research Institute

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: 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.

Date: 2017
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DOI: 10.1038/s41467-017-00101-w

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