ArticleJournal of virology2012
Herpes simplex virus 1 tegument protein US11 downmodulates the RLR signaling pathway via direct interaction with RIG-I and MDA-5.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 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
130 citing papers in PubMed, 171 citations in OpenAlex.
- Host Genetic Susceptibility and Antiviral Immunity Shape the Pathogenesis and Outcomes of Herpes Simplex Encephalitis.Biology · 2026Review
- SKP2 Regulates Pulmonary Inflammatory Injury Triggered by Bacterial Infection Through p27-Mediated Degradation of FOXN3.MedComm · 2026Article
- Duck plague virus US2 promotes p62-mediated autophagic degradation of RIG-I to suppress antiviral signaling.Poultry science · 2026Article
- IFI208, an interferon-stimulated gene, promotes host antiviral responses through liquid-liquid phase separation of MDA5.Nature communications · 2026Article
- Host Immune Response Mechanisms Against Herpes Simplex Virus Type 2 Infection.Pathogens (Basel, Switzerland) · 2026Review
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Divergent Strategies in Innate Immune Evasion: A Comparative Review of Three Alphaherpesvirus Subfamily Members-PRV, HSV-1, and VZV.Transboundary and emerging diseases · 2026Review
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- The Interplay Between Therapeutic Self-Amplifying RNA and the Innate Immune System: Balancing Efficiency and Reactogenicity.International journal of molecular sciences · 2025Review
- DEAD-box RNA helicase 10 inhibits porcine circovirus type 3 replication by interacting with the viral capsid protein and activating interferon responses.Journal of virology · 2025Article
- Direct relationship between protein expression and progeny yield of herpes simplex virus 1.mBio · 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
- ADAR1 p150 prevents HSV-1 from triggering PKR/eIF2α-mediated translational arrest and is required for efficient viral replication.PLoS pathogens · 2025Article
- ASFV pS183L protein negatively regulates RLR-mediated antiviral signalling by blocking MDA5 oligomerisation.Veterinary research · 2025Article
- Tackling cutaneous herpes simplex virus disease with topical immunomodulators-a call to action.Clinical microbiology reviews · 2025Review
- TRIM29 controls enteric RNA virus-induced intestinal inflammation by targeting NLRP6 and NLRP9b signaling pathways.Mucosal immunology · 2025Article
- Tug of war: innate immunity and herpes simplex keratitis.Frontiers in immunology · 2025Review
- When viral infections meet the anti-MDA5 antibody-positive dermatomyositis.Frontiers in immunology · 2025Review
- VZV IE4 downregulates cellular surface MHC-I via sequestering it to the Golgi complex.Cellular and molecular life sciences : CMLS · 2024Article
- Evasion of the Antiviral Innate Immunity by PRV.International journal of molecular sciences · 2024Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interferon (IFN)-mediated antiviral response is a major defense of the host immune system. In order to complete their life cycle, viruses must modulate host IFN-mediated immune responses. Herpes simplex virus 1 (HSV-1) is a large DNA virus containing more than 80 genes, many of which encode proteins that are involved in virus-host interactions and show immune modulatory capabilities. In this study, we demonstrate that the US11 protein, an RNA binding tegument protein of HSV-1, is a novel antagonist of the beta IFN (IFN-β) pathway. US11 significantly inhibited Sendai virus (SeV)-induced IFN-β production, and its double-stranded RNA (dsRNA) binding domain was indispensable for this inhibition activity. Additionally, wild-type HSV-1 coinfection showed stronger inhibition than US11 mutant HSV-1 in SeV-induced IFN-β production. Coimmunoprecipitation analysis demonstrated that the US11 protein in HSV-1-infected cells interacts with endogenous RIG-I and MDA-5 through its C-terminal RNA-binding domain, which was RNA independent. Expression of US11 in both transfected and HSV-1-infected cells interferes with the interaction between MAVS and RIG-I or MDA-5. Finally, US11 dampens SeV-mediated IRF3 activation. Taken together, the combined data indicate that HSV-1 US11 binds to RIG-I and MDA-5 and inhibits their downstream signaling pathway, preventing the production of IFN-β, which may contribute to the pathogenesis of HSV-1 infection.
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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 OpenQuestion graph.