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Species-Specific Deamidation of cGAS by Herpes Simplex Virus UL37 Protein Facilitates Viral Replication.

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机构： [1]Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA [2]School of Life Sciences, Hunan Normal University, Changsha, Hunan, China [3]Youjiang Medical University for Nationalities, Baise, Guangxi, China [4]The Fourth West China Hospital, Sichuan University, Chengdu, China [5]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, School of Basic Medical Sciences and Forensic Medicine, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, Sichuan 610041, China [6]Departments of Biological Sciences and Chemistry, University of Southern California, Los Angeles, CA 90089, USA [7]BioFrontiers Institute and Department of Molecular, Cellular, and Developmental Biology, University of Colorado Boulder, Boulder, CO 80303, USA [8]School of Life Sciences, Central South University, Changsha, Hunan 410008, China [9]Section of Infection and Immunity, Ostrow School of Dentistry, University of Southern California, Los Angeles, CA 90089-0641, USA

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Herpes simplex virus 1 (HSV-1) establishes infections in humans and mice, but some non-human primates exhibit resistance via unknown mechanisms. Innate immune recognition pathways are highly conserved but are pivotal in determining susceptibility to DNA virus infections. We report that variation of a single amino acid residue in the innate immune sensor cGAS determines species-specific inactivation by HSV-1. The HSV-1 UL37 tegument protein deamidates human and mouse cGAS. Deamidation impairs the ability of cGAS to catalyze cGAMP synthesis, which activates innate immunity. HSV-1 with deamidase-deficient UL37 promotes robust antiviral responses and is attenuated in mice in a cGAS- and STING-dependent manner. Mutational analyses identified a single asparagine in human and mouse cGAS that is not conserved in many non-human primates. This residue underpins UL37-mediated cGAS deamidation and species permissiveness of HSV-1. Thus, HSV-1 mediates cGAS deamidation for immune evasion and exploits species sequence variation to disarm host defenses. Copyright © 2018 Elsevier Inc. All rights reserved.

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出版当年[2018]版：

大类 | 1 区

生物

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最新[2023]版：

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医学

小类 | 1 区微生物学 1 区寄生虫学 1 区病毒学

第一作者：

第一作者机构： [1]Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA [9]Section of Infection and Immunity, Ostrow School of Dentistry, University of Southern California, Los Angeles, CA 90089-0641, USA

通讯作者：

通讯机构： [1]Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA [9]Section of Infection and Immunity, Ostrow School of Dentistry, University of Southern California, Los Angeles, CA 90089-0641, USA

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