ArticleCell insight2022
Herpes simplex virus protein UL56 inhibits cGAS-Mediated DNA sensing to evade antiviral immunity.
Article in Cell insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- The cGAS-STING signaling pathway in the regulation of pulmonary infections: a systematic review.Frontiers in cellular and infection microbiology · 2025Pooled it
- Structural and biochemical insights into the inhibition ofRSC chemical biology · 2026Article
- Alpha-herpesvirus US1 interacts with cGAS to suppress type I IFN responses and antiviral defense.PLoS pathogens · 2025Article
- Sensing of Ebinur Lake virus by distinct pattern recognition receptors dictates cell-type specific innate immunity and pathogenesis.Journal of virology · 2025Article
- Beyond interferons: Non-canonical roles of MITA/STING.Cell insight · 2025Review
- ATP2A2 regulates STING1/MITA-driven signal transduction including selective autophagy.Autophagy · 2025Article
- IRF1 amplifies HSV-1-triggered antiviral innate immunity in a feed-forward manner.Cell insight · 2025Article
- The conserved poxvirus membrane entry-fusion apparatus component OPG147 targets MITA/STING for immune evasion.PLoS pathogens · 2025Article
- HSV-1 UL56 protein recruits cellular NEDD4-family ubiquitin ligases to suppress CD1d expression and NKT cell function.Journal of virology · 2025Article
- Herpes simplex virus 1 encodes a STING antagonist that can be therapeutically targeted.Cell reports. Medicine · 2025Article
- Co-option of mitochondrial nucleic acid-sensing pathways by HSV-1 UL12.5 for reactivation from latent infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PLK2-mediated phosphorylation of SQSTM1 S349 promotes aggregation of polyubiquitinated proteins upon proteasomal dysfunction.Autophagy · 2024Article
- The monkeypox virus-host interplays.Cell insight · 2024Review
- Activation of the cGAS-STING-IRF3 Axis by Type I and II Interferons Contributes to Host Defense.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Co-option of mitochondrial nucleic acid sensing pathways by HSV-1 UL12.5 for reactivation from latent Infection.bioRxiv : the preprint server for biology · 2024Article
- HSV-1 employs UL56 to antagonize expression and function of cGAMP channels.Cell reports · 2024Article
- Review
- Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis.Pathogens (Basel, Switzerland) · 2023Review
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After herpes simplex virus type 1 (HSV-1) infection, the cytosolic sensor cyclic GMP-AMP synthase (cGAS) recognizes DNA and catalyzes synthesis of the second messenger 2'3'-cGAMP. cGAMP binds to the ER-localized adaptor protein MITA (also known as STING) to activate downstream antiviral responses. Conversely, HSV-1-encoded proteins evade antiviral immune responses via a wide variety of delicate mechanisms, promoting viral replication and pathogenesis. Here, we identified HSV-1 envelop protein UL56 as a negative regulator of cGAS-mediated innate immune responses. Overexpression of UL56 inhibited double-stranded DNA-triggered antiviral responses, whereas UL56-deficiency increased HSV-1-triggered induction of downstream antiviral genes. UL56-deficiency inhibited HSV-1 replication in wild-type but not MITA-deficient cells. UL56-deficient HSV-1 showed reduced replication in the brain of infected mice and was less lethal to infected mice. Mechanistically, UL56 interacted with cGAS and inhibited its DNA binding and enzymatic activity. Furthermore, we found that UL56 homologous proteins from different herpesviruses had similar roles in antagonizing cGAS-mediated innate immune responses. Our findings suggest that UL56 is a component of HSV-1 evasion of host innate immune responses by antagonizing the DNA sensor cGAS, which contributes to our understanding of the comprehensive mechanisms of immune evasion by herpesviruses.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.