Herpes Simplex Virus 1 UL36USP Antagonizes Type I Interferon-Mediated Antiviral Innate Immunity

Journal of Virology
Hui YuanChunfu Zheng

Abstract

Type I interferons (IFNs), as major components of the innate immune system, play a vital role in host resistance to a variety of pathogens. Canonical signaling mediated by type I IFNs activates the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway through binding to the IFN-α/β receptor (IFNAR), resulting in transcription of IFN-stimulated genes (ISGs). However, viruses have evolved multiple strategies to evade this process. Here, we report that herpes simplex virus 1 (HSV-1) ubiquitin-specific protease (UL36USP) abrogates the type I IFN-mediated signaling pathway independent of its deubiquitinase (DUB) activity. In this study, ectopically expressed UL36USP inhibited IFN-β-induced activation of ISRE promoter and transcription of ISGs, and overexpression of UL36USP lacking DUB activity did not influence this effect. Furthermore, UL36USP was demonstrated to antagonize IFN-β-induced activation of JAKs and STATs via specifically binding to the IFNAR2 subunit and blocking the interaction between JAK1 and IFNAR2. More importantly, knockdown of HSV-1 UL36USP restored the formation of JAK1-IFNAR2 complex. These findings underline the roles of UL36USP-IFNAR2 interaction in counteracting the type I IFN-medi...Continue Reading

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Citations

May 10, 2020·The Journal of Experimental Medicine·Chiranjeevi BoddaSøren R Paludan
Mar 7, 2019·Frontiers in Neurology·Elisa CaggiuLeonardo A Sechi
Dec 19, 2019·Frontiers in Microbiology·Yingying Lin, Chunfu Zheng
Oct 2, 2020·Microbiology and Molecular Biology Reviews : MMBR·Huifang Zhu, Chunfu Zheng
Jul 28, 2020·International Journal of Molecular Sciences·Kevin DanastasAnthony L Cunningham
Jan 10, 2021·International Journal of Molecular Sciences·Guendalina FroechlichNicola Zambrano
Nov 27, 2020·Frontiers in Immunology·Vivian LeiAmanda S MacLeod
Aug 10, 2021·Frontiers in Microbiology·Jingjing LiMeili Li

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