ArticleFrontiers in immunology2024
Pseudorabies virus tegument protein US2 antagonizes antiviral innate immunity by targeting cGAS-STING signaling pathway.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- The cGAS-STING/MITA pathway in innate antiviral immunity and beyond.Cell insight · 2026Review
- Isoliquiritigenin Elicits Potent Antiviral Activity Against Pseudorabies Virus Through Modulating the cGAS/STING and JAK/STAT Signaling Cascades.Veterinary sciences · 2026Article
- Unraveling the Multifaceted Role of TRIM21 in Virus-Triggered Innate Immunity and Diseases.Biomolecules · 2026Review
- Duck plague virus US2 promotes p62-mediated autophagic degradation of RIG-I to suppress antiviral signaling.Poultry science · 2026Article
- Duck plague virus LORF2 utilizes RNF34 to inhibit antiviral innate immunity by ubiquitination and degradation of IRF7.PLoS pathogens · 2026Article
- STING agonists as antiviral agents.FEBS letters · 2026Review
- 2'-5' Oligoadenylate Synthetase-Like 1- (OASL1-) deficient mice promote antiviral protection against pseudorabies virus infection associated with enhanced production of type I interferon.Scientific reports · 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
- Evaluation of a quintuple-gene-deleted PRV vector expressing PEDV S1: safety and immunogenicity in rabbits, mice, and piglets.Frontiers in microbiology · 2026Article
- cGAS-STING signaling pathway as a therapeutic target in human diseases.Chinese medical journal · 2025Review
- Pseudorabies virus DNA polymerase processivity factor pUL42 inhibits type I IFN production by negatively regulating cGAS-STING signaling pathway.Journal of virology · 2025Article
- PRV gD-Based DNA Vaccine Candidates Adjuvanted with cGAS, UniSTING, or IFN-α Enhance Protective Immunity.Pathogens (Basel, Switzerland) · 2025Article
- Drebrin Is Involved in the Life Cycle of Pseudorabies Virus by Regulating the Actin Cytoskeleton.Microorganisms · 2025Article
- BAG2 Inhibits Cervical Cancer Progression by Modulating Type I Interferon Signaling through Stabilizing STING.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Rosmarinic Acid inhibits Pseudorabies Virus (PRV) infection by activating the cGAS-STING signaling pathway.BMC microbiology · 2025Article
- Review
- Alphaherpesvirus in Pets and Livestock.Microorganisms · 2025Review
- RACK1 Associates With STING to Promote Type I Interferon Activation and Inhibit Pseudorabies Virus Infection.Transboundary and emerging diseases · 2025Article
- Evasion of the Antiviral Innate Immunity by PRV.International journal of molecular sciences · 2024Review
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Authors and funding
16 authors.
Funding
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Abstract
Background: The cGAS-STING axis-mediated type I interferon pathway is a crucial strategy for host defense against DNA virus infection. Numerous evasion strategies developed by the pseudorabies virus (PRV) counteract host antiviral immunity. To what extent PRV-encoded proteins evade the cGAS-STING signaling pathway is unknown. Methods: Using US2 stably expressing cell lines and US2-deficient PRV model, we revealed that the PRV tegument protein US2 reduces STING protein stability and downregulates STING-mediated antiviral signaling. Results: To promote K48-linked ubiquitination and STING degradation, US2 interacts with the LBD structural domain of STING and recruits the E3 ligase TRIM21. TRIM21 deficiency consistently strengthens the host antiviral immune response brought on by PRV infection. Additionally, US2-deficient PRV is less harmful in mice. Conclusions: Our study implies that PRV US2 inhibits IFN signaling by a new mechanism that selectively targets STING while successfully evading the host antiviral response. As a result, the present study reveals a novel strategy by which PRV evades host defense and offers explanations for why the Bartha-K61 classical vaccine strain failed to offer effective defense against PRV variant strains in China, indicating that US2 may be a key target for developing gene-deficient PRV vaccines.
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