ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Epstein-Barr Virus Expressed Long Non-Coding RNA (lncBARTs) Regulate EBV Latent Genome Replication.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026Review
- Epstein-Barr Virus Expressed Long Non-Coding RNA (lncBARTs) Regulate EBV Latent Genome Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The implications of FASN in viral infection and related diseases: a promising target in antiviral therapies.Frontiers in cellular and infection microbiology · 2026Review
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Authors and funding
13 authors.
Funding
Abstract
Epstein-Barr virus (EBV) is a ubiquitous human virus that is also linked to various human cancers. In EBV-associated nasopharyngeal carcinoma and gastric carcinoma cells, EBV expresses only essential viral antigens but high levels of long non-coding RNAs known as BamHI-A rightward transcripts (lncBARTs). The exact roles lncBARTs in the EBV life cycle and the development of EBV-associated cancers are largely not understood. This study demonstrates that lncBARTs play a role in maintaining viral genome replication by affecting the tethering of EBV oriP region to chromosome. Mechanistically, lncBARTs interact functionally with a complex consisting of Bromodomain-containing protein 4 (BRD4), CCTC-binding factor (CTCF), and EBV nuclear antigen 1 (EBNA1), anchoring their binding at oriP to facilitate EBV episome replication. Additionally, the lncBARTs-BRD4/CTCF complex contributes to the regulation of MYC and BCL2 expression. These findings suggest that lncBARTs modulate EBV latency through interactions with oriP region, while lncBARTs-BRD4/CTCF complexes promote host epigenome reprogramming and drive tumorigenesis in EBV-associated epithelial tumors.
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Registered trials
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