Interferon-stimulated TRIM69 interrupts dengue virus replication by ubiquitinating viral nonstructural protein 3

PLoS Pathogens
Kezhen WangJianfeng Dai

Abstract

In order to eliminate viral infections, hundreds of interferon-stimulated genes (ISGs) are induced via type I interferons (IFNs). However, the functions and mechanisms of most ISGs are largely unclear. A tripartite motif (TRIM) protein encoding gene TRIM69 is induced by dengue virus (DENV) infection as an ISG. TRIM69 restricts DENV replication, and its RING domain, which has the E3 ubiquitin ligase activity, is critical for its antiviral activity. An in vivo study further confirmed that TRIM69 contributes to the control of DENV infection in immunocompetent mice. Unlike many other TRIM family members, TRIM69 is not involved in modulation of IFN signaling. Instead, TRIM69 interacts with DENV Nonstructural Protein 3 (NS3) directly and mediates its polyubiquitination and degradation. Finally, Lys104 of NS3 is identified as the target of TRIM69-mediated ubiquitination. Our study demonstrates that TRIM69 restricts DENV replication by specifically ubiquitinating a viral nonstructural protein.

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Citations

Mar 5, 2019·PLoS Neglected Tropical Diseases·Chunling ZouJianfeng Dai
Oct 30, 2019·The Journal of General Virology·Adam Hage, Ricardo Rajsbaum
Aug 4, 2019·Journal of Virology·Suzannah J RihnSam J Wilson
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Mar 11, 2020·Virologica Sinica·Lionel Berthoux
Aug 25, 2020·Current Clinical Microbiology Reports·Maria I GiraldoRicardo Rajsbaum
Sep 18, 2020·Vaccines·Rosa C Coldbeck-ShackleyMichael R Beard
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Jan 6, 2021·International Journal of Molecular Sciences·Ramesh KumarSujatha Sunil
Feb 20, 2021·Virus Research·Debajit DeyS Saif Hasan
May 22, 2021·Frontiers in Microbiology·Haiyan YeLimin Chen

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Methods Mentioned

BETA
RNA-Seq
transfection
transfections
immunoprecipitation
confocal microscopy
pulldown
Co-IP
ubiquitination
Assay
co-immunoprecipitation

Software Mentioned

UbPred
Prism

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