ArticleJournal of virology2018
A Screen for Epstein-Barr Virus Proteins That Inhibit the DNA Damage Response Reveals a Novel Histone Binding Protein.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 40 citations in OpenAlex.
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Locus-specific proteomics identifies novel regulators of Epstein-Barr virus lytic reactivation.Journal of virology · 2026Article
- Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.bioRxiv : the preprint server for biology · 2025Article
- Epigenetic drugs against human DNA viruses and retroviruses.Antiviral research · 2025Review
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- The immediate-early protein 1 of human herpesvirus 6B interacts with NBS1 and inhibits ATM signaling.EMBO reports · 2024Article
- The interplay between viral molecular mimicry and host chromatin dynamics.Nucleus (Austin, Tex.) · 2023Review
- Changes in SUMO-modified proteins in Epstein-Barr virus infection identifies reciprocal regulation of TRIM24/28/33 complexes and the lytic switch BZLF1.PLoS pathogens · 2023Article
- Feature Reviews of the Molecular Mechanisms of Nasopharyngeal Carcinoma.Biomedicines · 2023Review
- Contribution of Epstein-Barr Virus Lytic Proteins to Cancer Hallmarks and Implications from Other Oncoviruses.Cancers · 2023Review
- Epstein-Barr Virus History and Pathogenesis.Viruses · 2023Review
- GJournal of virology · 2022Article
- MC180295 Inhibited Epstein-Barr Virus-Associated Gastric Carcinoma Cell Growth by Suppressing DNA Repair and the Cell Cycle.International journal of molecular sciences · 2022Article
- Epstein-Barr virus protein BKRF4 restricts nucleosome assembly to suppress host antiviral responses.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The ORF45 Protein of Kaposi's Sarcoma-Associated Herpesvirus and Its Critical Role in the Viral Life Cycle.Viruses · 2022Review
- Comprehensive Analyses of Intraviral Epstein-Barr Virus Protein-Protein Interactions Hint Central Role of BLRF2 in the Tegument Network.Journal of virology · 2022Article
- Replication Compartments-The Great Survival Strategy for Epstein-Barr Virus Lytic Replication.Microorganisms · 2022Review
- Epstein-Barr Virus BGLF2 commandeers RISC to interfere with cellular miRNA function.PLoS pathogens · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
To replicate and persist in human cells, linear double-stranded DNA (dsDNA) viruses, such as Epstein-Barr virus (EBV), must overcome the host DNA damage response (DDR) that is triggered by the viral genomes. Since this response is necessary to maintain cellular genome integrity, its inhibition by EBV is likely an important factor in the development of cancers associated with EBV infection, including gastric carcinoma. Here we present the first extensive screen of EBV proteins that inhibit dsDNA break signaling. We identify the BKRF4 tegument protein as a DDR inhibitor that interferes with histone ubiquitylation at dsDNA breaks and recruitment of the RNF168 histone ubiquitin ligase. We further show that BKRF4 binds directly to histones through an acidic domain that targets BKRF4 to cellular chromatin and is sufficient to inhibit dsDNA break signaling. BKRF4 transcripts were detected in EBV-positive gastric carcinoma cells (AGS-EBV), and these increased in lytic infection. Silencing of BKRF4 in both latent and lytic AGS-EBV cells (but not in EBV-negative AGS cells) resulted in increased dsDNA break signaling, confirming a role for BKRF4 in DDR inhibition in the context of EBV infection and suggesting that BKRF4 is expressed in latent cells. BKRF4 was also found to be consistently expressed in EBV-positive gastric tumors in the absence of a full lytic infection. The results suggest that BKRF4 plays a role in inhibiting the cellular DDR in latent and lytic EBV infection and that the resulting accumulation of DNA damage might contribute to development of gastric carcinoma.
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