ArticleNucleic acids research2014
Epstein-Barr virus-mediated transformation of B cells induces global chromatin changes independent to the acquisition of proliferation.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Omics-Level Approaches to Studying Gammaherpesvirus Infection.Pathogens (Basel, Switzerland) · 2026Review
- Epstein-Barr virus hijacks histone demethylase machinery to drive epithelial malignancy progression through KDM5B upregulation.Signal transduction and targeted therapy · 2025Article
- Epstein-Barr virus infection: the micro and macro worlds.Virology journal · 2023Review
- Epstein-Barr virus evades restrictive host chromatin closure by subverting B cell activation and germinal center regulatory loci.Cell reports · 2023Article
- Epstein-Barr Virus (EBV) Epithelial Associated Malignancies: Exploring Pathologies and Current Treatments.International journal of molecular sciences · 2022Review
- Genome-wide association study identifies Sjögren's risk loci with functional implications in immune and glandular cells.Nature communications · 2022Article
- Variants on the UBE2L3/YDJC Autoimmune Disease Risk Haplotype Increase UBE2L3 Expression by Modulating CCCTC-Binding Factor and YY1 Binding.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- Review
- Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021Review
- Interaction sites of the Epstein-Barr virus Zta transcription factor with the host genome in epithelial cells.Access microbiology · 2021Article
- The Impact of Epstein-Barr Virus Infection on Epigenetic Regulation of Host Cell Gene Expression in Epithelial and Lymphocytic Malignancies.Frontiers in oncology · 2021Review
- Review
- Dynamic chromatin accessibility profiling reveals changes in host genome organization in response to baculovirus infection.PLoS pathogens · 2020Article
- EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Mechanisms of B-Cell Oncogenesis Induced by Epstein-Barr Virus.Journal of virology · 2019Review
- Enhancer histone-QTLs are enriched on autoimmune risk haplotypes and influence gene expression within chromatin networks.Nature communications · 2018Article
- Epstein-Barr virus: a master epigenetic manipulator.Current opinion in virology · 2017Review
- Regulatory network changes between cell lines and their tissues of origin.BMC genomics · 2017Article
- Regulation of tumour related genes by dynamic epigenetic alteration at enhancer regions in gastric epithelial cells infected by Epstein-Barr virus.Scientific reports · 2017Article
- Epstein-Barr Virus Oncoprotein LMP1 Mediates Epigenetic Changes in Host Gene Expression through PARP1.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Epstein-Barr virus (EBV) infects and transforms human primary B cells inducing indefinite proliferation. To investigate the potential participation of chromatin mechanisms during the EBV-mediated transformation of resting B cells we performed an analysis of global changes in histone modifications. We observed a remarkable decrease and redistribution of heterochromatin marks including H4K20me3, H3K27me3 and H3K9me3. Loss of H4K20me3 and H3K9me3 occurred at constitutive heterochromatin repeats. For H3K27me3 and H3K9me3, comparison of ChIP-seq data revealed a decrease in these marks in thousands of genes, including clusters of HOX and ZNF genes, respectively. Moreover, DNase-seq data comparison between resting and EBV-transformed B cells revealed increased endonuclease accessibility in thousands of genomic sites. We observed that both loss of H3K27me3 and increased accessibility are associated with transcriptional activation. These changes only occurred in B cells transformed with EBV and not in those stimulated to proliferate with CD40L/IL-4, despite their similarities in the cell pathways involved and proliferation rates. In fact, B cells infected with EBNA-2 deficient EBV, which have much lower proliferation rates, displayed similar decreases for heterochromatic histone marks. Our study describes a novel phenomenon related to transformation of B cells, and highlights its independence of the pure acquisition of proliferation.
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