ArticleNucleic acids research2023
The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 22 citations in OpenAlex.
- Spatial specificity of Epstein-Barr virus infection in gastric cancer: A 44-case clinicopathological analysis.Experimental and therapeutic medicine · 2026Article
- Hybrid extrachromosomal DNA in HPV-driven cancers.Journal of virology · 2026Review
- Omics-Level Approaches to Studying Gammaherpesvirus Infection.Pathogens (Basel, Switzerland) · 2026Review
- EBNA1 inhibitors reveal CDC7 and POU2F1 as direct functional targets in EBV epithelial cancers.mBio · 2026Article
- Recent advances in Epstein-Barr virus vaccines development from mechanistic exploration to clinical translation.NPJ vaccines · 2026Review
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- Epstein-Barr Virus Expressed Long Non-Coding RNA (lncBARTs) Regulate EBV Latent Genome Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Association of hepatitis B virus genomes with active chromatin hubs challenges host replication fidelity, leading to DNA damage.Journal of virology · 2025Article
- Integrated transcriptomic and methylome analysis reveals retinoic acid pathway activation after decitabine treatment in EBV associated gastric cancer.bioRxiv : the preprint server for biology · 2025Article
- Multiple long-rangemBio · 2025Article
- MUC1-C auto-regulatory complex with EBNA1 is responsible for latent Epstein-Barr virus-associated gastric cancer progression.Oncogene · 2025Article
- Histone variant H2A.Z cooperates with EBNA1 to maintain Epstein-Barr virus latent epigenome.mBio · 2025Article
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- Landscape of the Epstein-Barr virus-host chromatin interactome and gene regulation.The EMBO journal · 2025Article
- EBNA leader protein orchestrates chromatin architecture remodeling during Epstein-Barr virus-induced B cell transformation.Nucleic acids research · 2025Article
- The HSV-1 encoded CCCTC-binding factor, CTRL2, impacts the nature of viral chromatin during HSV-1 lytic infection.PLoS pathogens · 2024Article
- The DNA loop release factor WAPL suppresses Epstein-Barr virus latent membrane protein expression to maintain the highly restricted latency I program.PLoS pathogens · 2024Article
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Epstein-Barr virus (EBV) establishes lifelong asymptomatic infection by replication of its chromatinized episomes with the host genome. EBV exhibits different latency-associated transcriptional repertoires, each with distinct three-dimensional structures. CTCF, Cohesin and PARP1 are involved in maintaining viral latency and establishing episome architecture. Epstein-Barr virus-associated gastric cancer (EBVaGC) represents 1.3-30.9% of all gastric cancers globally. EBV-positive gastric cancers exhibit an intermediate viral transcription profile known as 'Latency II', expressing specific viral genes and noncoding RNAs. In this study, we investigated the impact of PARP1 inhibition on CTCF/Cohesin binding in Type II latency. We observed destabilization of the binding of both factors, leading to a disrupted three-dimensional architecture of the episomes and an altered viral gene expression. Despite sharing the same CTCF binding profile, Type I, II and III latencies exhibit different 3D structures that correlate with variations in viral gene expression. Additionally, our analysis of H3K27ac-enriched interactions revealed differences between Type II latency episomes and a link to cellular transformation through docking of the EBV genome at specific sites of the Human genome, thus promoting oncogene expression. Overall, this work provides insights into the role of PARP1 in maintaining active latency and novel mechanisms of EBV-induced cellular transformation.
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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.