ArticleJournal of virology2012
Epigenetic histone modification of Epstein-Barr virus BZLF1 promoter during latency and reactivation in Raji cells.
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 85 papers.
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Who cites it
85 citing papers in PubMed, 117 citations in OpenAlex.
- Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas.Npj viruses · 2026Article
- Proteomic screening identifies HNRNPA2B1 as an epigenetic repressor of Epstein-Barr virus reactivation.Journal of virology · 2026Article
- EBNA1 inhibitors reveal CDC7 and POU2F1 as direct functional targets in EBV epithelial cancers.mBio · 2026Article
- Reactivation and Management of Endogenous Latent Herpesviruses in the Spaceflight Environment.Current microbiology · 2026Review
- Locus-specific proteomics identifies novel regulators of Epstein-Barr virus lytic reactivation.Journal of virology · 2026Article
- Fueling silence: Metabolic control of latent viral infection.PLoS pathogens · 2026Article
- Proteomic Screening Identifies HNRNPA2B1 as an Epigenetic Repressor of Epstein-Barr Virus Reactivation.bioRxiv : the preprint server for biology · 2026Article
- Inhibition of KDM5A/B promotes antitumor innate immune responses in HHV-8/KSHV-positive B-cell lymphomas.bioRxiv : the preprint server for biology · 2026Article
- The microbiome-EBV axis in carcinogenesis bridges commensal influence and viral oncogenesis.Frontiers in immunology · 2026Review
- The role ofFrontiers in oncology · 2026Review
- Synergistic carcinogenesis of the nasopharyngeal microbiome and Epstein-Barr virus: mechanisms of metabolic reprogramming and immune evasion.Frontiers in immunology · 2026Review
- Epstein-Barr virus: biology, pathogenesis and therapy of lymphomas.Discover oncology · 2025Review
- Model Systems of Gammaherpesvirus Infection, Immunity, and Disease.Journal of medical virology · 2025Review
- Histone variant H2A.Z cooperates with EBNA1 to maintain Epstein-Barr virus latent epigenome.mBio · 2025Article
- E2F1 suppresses Epstein-Barr virus lytic reactivation through cellular and viral transcriptional networks.PLoS pathogens · 2025Article
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- A Liposome-Based Nanoparticle Vaccine Induces Effective Immunity Against EBV Infection.Vaccines · 2025Article
- The nucleic acid binding protein SFPQ represses EBV lytic reactivation by promoting histone H1 expression.Nature communications · 2024Article
- Awakening the sleeping giant: Epstein-Barr virus reactivation by biological agents.Pathogens and disease · 2024Review
- Histone methylation in Epstein-Barr virus-associated diseases.Epigenomics · 2024Review
25 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Epstein-Barr virus (EBV) predominantly establishes latent infection in B cells, and the reactivation of the virus from latency is dependent on the expression of the viral BZLF1 protein. The BZLF1 promoter (Zp) normally exhibits only low basal activity but is activated in response to chemical or biological inducers, such as 12-O-tetradecanoylphorbol-13-acetate (TPA), calcium ionophores, or histone deacetylase (HDAC) inhibitors. In some cell lines latently infected with EBV, an HDAC inhibitor alone can induce BZLF1 transcription, while the treatment does not enhance expression in other cell lines, such as B95-8 or Raji cells, suggesting unknown suppressive mechanisms besides histone deacetylation in those cells. Here, we found the epigenetic modification of the BZLF1 promoter in latent Raji cells by histone H3 lysine 27 trimethylation (H3K27me3), H3K9me2/me3, and H4K20me3. Levels of active markers such as histone acetylation and H3K4me3 were low in latent cells but increased upon reactivation. Treatment with 3-deazaneplanocin A (DZNep), an inhibitor of H3K27me3 and H4K20me3, significantly enhanced the BZLF1 transcription in Raji cells when in combination with an HDAC inhibitor, trichostatin A (TSA). The knockdown of Ezh2 or Suv420h1, histone methyltransferases for H3K27me3 or H4K20me3, respectively, further proved the suppression of Zp by the methylations. Taken together, the results indicate that H3K27 methylation and H4K20 methylation are involved, at least partly, in the maintenance of latency, and histone acetylation and H3K4 methylation correlate with the reactivation of the virus in Raji cells.
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