ArticlePLoS pathogens2011
EBV tegument protein BNRF1 disrupts DAXX-ATRX to activate viral early gene transcription.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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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Who cites it
91 citing papers in PubMed, 131 citations in OpenAlex.
- Epstein-Barr Virus-host epigenetic interplay: mechanisms of regulation and therapeutic potential.Clinical epigenetics · 2026Review
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- Molecular mechanisms of Epstein-Barr Virus in the pathogenesis of lymphomas and new opportunities for precision medicine.Discover oncology · 2026Review
- Lysine-specific histone demethylase complex restricts Epstein-Barr virus lytic reactivation.Nature microbiology · 2025Article
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- Sp140L functions as a herpesvirus restriction factor suppressing viral transcription and activating interferon-stimulated genes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.Tumour virus research · 2025Review
- Gastric carcinoma harbouring loss‑of‑function mutations in theOncology letters · 2025Article
- The elevated expression of ORF75, a KSHV lytic gene, in Kaposi sarcoma lesions is driven by a GC-rich DNA cis element in its promoter region.PLoS pathogens · 2025Article
- Research landmarks on the 60th anniversary of Epstein-Barr virus.Science China. Life sciences · 2025Review
- A single-cell atlas of the Culex tarsalis midgut during West Nile virus infection.PLoS pathogens · 2025Article
- A single-cell atlas of thebioRxiv : the preprint server for biology · 2024Article
- ATRX restricts Human Cytomegalovirus (HCMV) viral DNA replication through heterochromatinization and minimizes unpackaged viral genomes.PLoS pathogens · 2024Article
- The nucleic acid binding protein SFPQ represses EBV lytic reactivation by promoting histone H1 expression.Nature communications · 2024Article
- Current Insights into the Maturation of Epstein-Barr Virus Particles.Microorganisms · 2024Review
- Epstein-Barr virus lytic gene BNRF1 promotes B-cell lymphomagenesis via IFI27 upregulation.PLoS pathogens · 2024Article
- Review
- MORC3 represses the HCMV major immediate early promoter in myeloid cells in the absence of PML nuclear bodies.Journal of medical virology · 2023Article
- Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Productive infection by herpesviruses involve the disabling of host-cell intrinsic defenses by viral encoded tegument proteins. Epstein-Barr Virus (EBV) typically establishes a non-productive, latent infection and it remains unclear how it confronts the host-cell intrinsic defenses that restrict viral gene expression. Here, we show that the EBV major tegument protein BNRF1 targets host-cell intrinsic defense proteins and promotes viral early gene activation. Specifically, we demonstrate that BNRF1 interacts with the host nuclear protein Daxx at PML nuclear bodies (PML-NBs) and disrupts the formation of the Daxx-ATRX chromatin remodeling complex. We mapped the Daxx interaction domain on BNRF1, and show that this domain is important for supporting EBV primary infection. Through reverse transcription PCR and infection assays, we show that BNRF1 supports viral gene expression upon early infection, and that this function is dependent on the Daxx-interaction domain. Lastly, we show that knockdown of Daxx and ATRX induces reactivation of EBV from latently infected lymphoblastoid cell lines (LCLs), suggesting that Daxx and ATRX play a role in the regulation of viral chromatin. Taken together, our data demonstrate an important role of BNRF1 in supporting EBV early infection by interacting with Daxx and ATRX; and suggest that tegument disruption of PML-NB-associated antiviral resistances is a universal requirement for herpesvirus infection in the nucleus.
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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.