ArticleJournal of virology2022
The US3 Kinase of Herpes Simplex Virus Phosphorylates the RNA Sensor RIG-I To Suppress Innate Immunity.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 27 citations in OpenAlex.
- Alpha-herpesvirus UL55 synergizes with ICP27 to suppress type I interferon production through conserved and host-adapted mechanisms.Journal of virology · 2026Article
- Identification of UL3.5 as a novel substrate of DPV US3 kinase whose phosphorylation at Ser64/Ser84 enhances protein stability and promotes viral release, and cell-to-cell spread.Poultry science · 2026Article
- Article
- The PI3K/Akt Pathway in Herpesvirus Biology: A Double-Edged Sword in Host-Virus Interactions.Microorganisms · 2026Review
- RNF20 dynamically regulates RIG-I and MDA5 transcription and degradation via nucleocytoplasmic translocation to balance antiviral signaling.PLoS pathogens · 2026Article
- Divergent Strategies in Innate Immune Evasion: A Comparative Review of Three Alphaherpesvirus Subfamily Members-PRV, HSV-1, and VZV.Transboundary and emerging diseases · 2026Review
- Engineered Protein Modification: A New Paradigm for Enhancing Biosensing Sensitivity and Diagnostic Accuracy.Biosensors · 2025Review
- HSV-1 US3: A Master Mimic Hijacking Host Kinase Networks for Viral Dominance.Journal of medical virology · 2025Review
- TRIM23 mediates cGAS-induced autophagy in anti-HSV defense.Nature communications · 2025Article
- Understanding the interplay between oHSV and the host immune system: Implications for therapeutic oncolytic virus development.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Review
- Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity.Frontiers in microbiology · 2025Review
- Article
- Review
- The TET3 inflammasome senses unique long HSV-1 proteins for virus particle budding from the nucleus.Cellular & molecular immunology · 2024Article
- Impaired endocytosis and accumulation in early endosomal compartments defines herpes simplex virus-mediated disruption of the nonclassical MHC class I-related molecule MR1.The Journal of biological chemistry · 2024Article
- A review of HSV pathogenesis, vaccine development, and advanced applications.Molecular biomedicine · 2024Review
- 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
- Advances in the immunoescape mechanisms exploited by alphaherpesviruses.Frontiers in microbiology · 2024Review
- The precise function of alphaherpesvirus tegument proteins and their interactions during the viral life cycle.Frontiers in microbiology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent studies have demonstrated that the signaling activity of the cytosolic pathogen sensor retinoic acid-inducible gene-I (RIG-I) is modulated by a variety of posttranslational modifications (PTMs) to fine-tune the antiviral type I interferon (IFN) response. Whereas K63-linked ubiquitination of the RIG-I caspase activation and recruitment domains (CARDs) catalyzed by TRIM25 or other E3 ligases activates RIG-I, phosphorylation of RIG-I at S8 and T170 represses RIG-I signal transduction by preventing the TRIM25-RIG-I interaction and subsequent RIG-I ubiquitination. While strategies to suppress RIG-I signaling by interfering with its K63-polyubiquitin-dependent activation have been identified for several viruses, evasion mechanisms that directly promote RIG-I phosphorylation to escape antiviral immunity are unknown. Here, we show that the serine/threonine (Ser/Thr) kinase US3 of herpes simplex virus 1 (HSV-1) binds to RIG-I and phosphorylates RIG-I specifically at S8. US3-mediated phosphorylation suppressed TRIM25-mediated RIG-I ubiquitination, RIG-I-MAVS binding, and type I IFN induction. We constructed a mutant HSV-1 encoding a catalytically-inactive US3 protein (K220A) and found that, in contrast to the parental virus, the US3 mutant HSV-1 was unable to phosphorylate RIG-I at S8 and elicited higher levels of type I IFNs, IFN-stimulated genes (ISGs), and proinflammatory cytokines in a RIG-I-dependent manner. Finally, we show that this RIG-I evasion mechanism is conserved among the alphaherpesvirus US3 kinase family. Collectively, our study reveals a novel immune evasion mechanism of herpesviruses in which their US3 kinases phosphorylate the sensor RIG-I to keep it in the signaling-repressed state.
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What Socratic holds
Registered trials
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 Socratic graph.