ArticleMolecular and cellular biology1997
Host-cell-determined methylation of specific Epstein-Barr virus promoters regulates the choice between distinct viral latency programs.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 82 citations in OpenAlex.
- A thorough insight into the life cycle of the Epstein-Barr virus. From the molecular to the organismal level.Current research in microbial sciences · 2025Review
- Review
- Navigating Latency-Inducing Viral Infections: Therapeutic Targeting and Nanoparticle Utilization.Biomaterials research · 2024Review
- Epigenetic and epitranscriptomic regulation during oncogenicFrontiers in microbiology · 2024Review
- Targeting the crosstalk of epigenetic modifications and immune evasion in nasopharyngeal cancer.Cell biology and toxicology · 2023Review
- Review
- Case Report: Primary Immunodeficiencies, Massive EBV+ T-Cell Lympoproliferation Leading to the Diagnosis of ICF2 Syndrome.Frontiers in immunology · 2021Article
- DNA methylation enzymes and PRC1 restrict B-cell Epstein-Barr virus oncoprotein expression.Nature microbiology · 2020Article
- Regulation of Epstein-Barr Virus Life Cycle and Cell Proliferation by Histone H3K27 Methyltransferase EZH2 in Akata Cells.mSphere · 2018Article
- Epigenetic crossroads of the Epstein-Barr virus B-cell relationship.Current opinion in virology · 2018Review
- Article
- Identification of Novel Kaposi's Sarcoma-Associated Herpesvirus Orf50 Transcripts: Discovery of New RTA Isoforms with Variable Transactivation Potential.Journal of virology · 2017Article
- Identification of alternative transcripts encoding the essential murine gammaherpesvirus lytic transactivator RTA.Journal of virology · 2014Article
- Epigenetic regulation of EBV and KSHV latency.Current opinion in virology · 2013Review
- Latency of Epstein-Barr virus is disrupted by gain-of-function mutant cellular AP-1 proteins that preferentially bind methylated DNA.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The B cell transcription program mediates hypomethylation and overexpression of key genes in Epstein-Barr virus-associated proliferative conversion.Genome biology · 2013Article
- BZLF1 governs CpG-methylated chromatin of Epstein-Barr Virus reversing epigenetic repression.PLoS pathogens · 2012Article
- The lytic phase of epstein-barr virus requires a viral genome with 5-methylcytosine residues in CpG sites.Journal of virology · 2012Article
- trans-Repression of protein expression dependent on the Epstein-Barr virus promoter Wp during latency.Journal of virology · 2011Article
- CpG-methylation regulates a class of Epstein-Barr virus promoters.PLoS pathogens · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) is capable of adopting three distinct forms of latency: the type III latency program, in which six EBV-encoded nuclear antigens (EBNAs) are expressed, and the type I and type II latency programs, in which only a single viral nuclear protein, EBNA1, is produced. Several groups have reported heavy CpG methylation of the EBV genome in Burkitt's lymphoma cell lines which maintain type I latency, and loss of viral genome methylation in tumor cell lines has been correlated with a switch to type III latency. Here, evidence that the type III latency program must be inactivated by methylation to allow EBV to enter the type I or type II restricted latency program is provided. The data demonstrates that the EBNA1 gene promoter, Qp, active in types I and II latency, is encompassed by a CpG island which is protected from methylation. CpG methylation inactivates the type III latency program and consequently allows the type I or II latency program to operate by alleviating EBNA1-mediated repression of Qp. Methylation of the type III latency EBNA gene promoter, Cp, appears to be essential to prevent type III latency, since EBNA1 is expressed in all latently infected cells and, as shown here, is the only viral antigen required for activation of Cp. EBV is thus a pathogen which subverts host-cell-determined methylation to regulate distinct genetic programs.
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Registered trials
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 OpenQuestion graph.