ArticlePLoS pathogens2023
Suppression of cGAS- and RIG-I-mediated innate immune signaling by Epstein-Barr virus deubiquitinase BPLF1.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The ubiquitin-proteasome system is an important driver of EBV-associated nasopharyngeal carcinoma progression: a meta-analysis of transcriptomic data.Scientific reports · 2026Pooled it
- The Significance of cGAS-STING Signaling in Response to Oncogenic Viruses.Cell biochemistry and function · 2026Review
- Alpha-herpesvirus UL55 synergizes with ICP27 to suppress type I interferon production through conserved and host-adapted mechanisms.Journal of virology · 2026Article
- EBV (LMP1) enhances cisplatin resistance by enhancing degradation of interferon regulatory factor 3.Cell communication and signaling : CCS · 2026Article
- Roles of the cGAS-STING signaling pathway in viral latency.Journal of virology · 2026Review
- EBV Triggers a Distinct Antiviral Response in HMC3 Cells.bioRxiv : the preprint server for biology · 2026Article
- A System-Level Perspective on Epstein-Barr Virus Persistence: The Partial Lytic Reactivation.International journal of molecular sciences · 2026Review
- STING agonists as antiviral agents.FEBS letters · 2026Review
- The segmented flavivirus ALSV-encoded nucleoprotein VP2 inhibits type I interferon production by targeting RIG-I.Microbiology spectrum · 2026Article
- Zinc pyrithione functions as a small-molecule STING agonist to exert antitumor immunotherapy effects.Acta pharmacologica Sinica · 2026Article
- STING single amino acid polymorphisms modulate iridovirus immune evasion and pathogenicity spectrum.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Epstein-Barr virus associated diseases: Immune alterations and targeted approaches.Frontiers in immunology · 2026Review
- EBV-associated gastric carcinoma occurring one year after metabolic bariatric surgery: case report and literature review.Frontiers in oncology · 2026Article
- Genome-wide association study identifies and validates genetic variation in the RIG-I/MAVS signaling pathway associated with HIV-related Kaposi sarcoma in children and adults.Frontiers in oncology · 2026Article
- STING inhibits viral lytic reactivation and cell growth in primary effusion lymphoma.Frontiers in immunology · 2026Article
- mRNA Cancer Vaccines: From Pandemic Paradigm to Personalized Oncology Therapeutics.Cancer innovation · 2025Review
- Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2.Emerging microbes & infections · 2025Article
- Extracellular vesicles derived EBV tegument protein BRRF2 suppresses cGAS phase separation to promote anti-viral innate immune evasion.Nature communications · 2025Article
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Targeting the cGAS-STING Pathway to Modulate Immune Inflammation in Diabetes and Cardiovascular Complications: Mechanisms and Therapeutic Insights.Current issues in molecular biology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV) has developed effective strategies to evade host innate immune responses. Here we reported on mitigation of type I interferon (IFN) production by EBV deubiquitinase (DUB) BPLF1 through cGAS-STING and RIG-I-MAVS pathways. The two naturally occurring forms of BPLF1 exerted potent suppressive effect on cGAS-STING-, RIG-I- and TBK1-induced IFN production. The observed suppression was reversed when DUB domain of BPLF1 was rendered catalytically inactive. The DUB activity of BPLF1 also facilitated EBV infection by counteracting cGAS-STING- and TBK1-mediated antiviral defense. BPLF1 associated with STING to act as an effective DUB targeting its K63-, K48- and K27-linked ubiquitin moieties. BPLF1 also catalyzed removal of K63- and K48-linked ubiquitin chains on TBK1 kinase. The DUB activity of BPLF1 was required for its suppression of TBK1-induced IRF3 dimerization. Importantly, in cells stably carrying EBV genome that encodes a catalytically inactive BPLF1, the virus failed to suppress type I IFN production upon activation of cGAS and STING. This study demonstrated IFN antagonism of BPLF1 mediated through DUB-dependent deubiquitination of STING and TBK1 leading to suppression of cGAS-STING and RIG-I-MAVS signaling.
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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 Socratic graph.