ArticleFrontiers in genetics2013
Epigenetic modification of the Epstein-Barr virus BZLF1 promoter regulates viral reactivation from latency.
Article in Frontiers in genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- A System-Level Perspective on Epstein-Barr Virus Persistence: The Partial Lytic Reactivation.International journal of molecular sciences · 2026Review
- PARP1 Inhibition Halts EBV+ Lymphoma Progression by Disrupting the EBNA2/MYC Axis.Journal of medical virology · 2025Article
- Histone methylation in Epstein-Barr virus-associated diseases.Epigenomics · 2024Review
- Targeting the crosstalk of epigenetic modifications and immune evasion in nasopharyngeal cancer.Cell biology and toxicology · 2023Review
- Three-Dimensional Chromatin Structure of the EBV Genome: A Crucial Factor in Viral Infection.Viruses · 2023Review
- Methionine metabolism controls the B cell EBV epigenome and viral latency.Cell metabolism · 2022Article
- Andrographolide Inhibits Epstein-Barr Virus Lytic Reactivation in EBV-Positive Cancer Cell Lines through the Modulation of Epigenetic-Related Proteins.Molecules (Basel, Switzerland) · 2022Article
- Dual Role of YY1 in HPV Life Cycle and Cervical Cancer Development.International journal of molecular sciences · 2022Review
- Role of DNA Methylation and CpG Sites in the Viral Telomerase RNA Promoter during Gallid Herpesvirus 2 Pathogenesis.Journal of virology · 2020Article
- Epstein-Barr Virus Early Protein BFRF1 Suppresses IFN-β Activity by Inhibiting the Activation of IRF3.Frontiers in immunology · 2020Article
- An Epigenetic Journey: Epstein-Barr Virus Transcribes Chromatinized and Subsequently Unchromatinized Templates during Its Lytic Cycle.Journal of virology · 2019Review
- Pathogenesis of Human Gammaherpesviruses: Recent Advances.Current clinical microbiology reports · 2019Article
- Regulation of Epstein-Barr Virus Life Cycle and Cell Proliferation by Histone H3K27 Methyltransferase EZH2 in Akata Cells.mSphere · 2018Article
- Mechanism of activation of the BNLF2a immune evasion gene of Epstein-Barr virus by Zta.The Journal of general virology · 2018Article
- The Epstein-Barr Virus BRRF1 Gene Is Dispensable for Viral Replication in HEK293 cells and Transformation.Scientific reports · 2017Article
- Article
- ERK/c-Jun Recruits Tet1 to Induce Zta Expression and Epstein-Barr Virus Reactivation through DNA Demethylation.Scientific reports · 2016Article
- The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016Review
- Epigenetics and animal virus infections.Frontiers in genetics · 2015Article
- Keeping it quiet: chromatin control of gammaherpesvirus latency.Nature reviews. Microbiology · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Epstein-Barr virus (EBV) is an oncogenic human gamma-herpesvirus that predominantly establishes latent infection in B lymphocytes. Viral genomes exist as extrachromosomal episomes with a nucleosomal structure. Maintenance of virus latency or execution of reactivation is controlled by the expression of BZLF1, a viral immediate-early gene product, tightly controlled at the transcriptional level. In this article, we review how BZLF1 transcription is controlled, in other words how virus reactivation is regulated, especially in terms of epigenetics. We recently found that histone H3 lysine 27 trimethylation (H3K27me3) and H4K20me3 markers are crucial for suppression of BZLF1 in latent Raji cells. In addition, H3K9me2/3, heterochromatin protein 1, and H2A ubiquitination are associated with latency, whereas positive markers, such as higher histone acetylation and H3K4me3, are concomitant with reactivation. Since lytic replication eventually causes cell cycle arrest and cell death, development of oncolytic therapy for EBV-positive cancers is conceivable using epigenetic disruptors. In addition, we note the difficulties in analyzing roles of epigenetics in EBV, including issues like cell type dependence and virus copy numbers.
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