ArticleVirology2017
PARP1 restricts Epstein Barr Virus lytic reactivation by binding the BZLF1 promoter.
Article in Virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 44 citations in OpenAlex.
- A System-Level Perspective on Epstein-Barr Virus Persistence: The Partial Lytic Reactivation.International journal of molecular sciences · 2026Review
- Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.bioRxiv : the preprint server for biology · 2026Article
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Relationship between Epstein-Barr virus and inflammatory bowel disease.World journal of gastroenterology · 2025Review
- Epstein-Barr Virus Encoded lncRNAs Control the Viral Lytic Switch.bioRxiv : the preprint server for biology · 2025Article
- AAV Kills Dividing Cells by Depleting PARP1 and Other DNA Damage Response Proteins.bioRxiv : the preprint server for biology · 2025Article
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- PARP1 Inhibition Halts EBV+ Lymphoma Progression by Disrupting the EBNA2/MYC Axis.Journal of medical virology · 2025Article
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- PARP1 as an Epigenetic Modulator: Implications for the Regulation of Host-Viral Dynamics.Pathogens (Basel, Switzerland) · 2024Review
- Hypocortisolemic ASIA: a vaccine- and chronic infection-induced syndrome behind the origin of long COVID and myalgic encephalomyelitis.Frontiers in immunology · 2024Review
- Identifying the key regulators orchestrating Epstein-Barr virus reactivation.Frontiers in microbiology · 2024Review
- Targeting latent viral infection in EBV-associated lymphomas.Frontiers in immunology · 2024Review
- The three-dimensional structure of the EBV genome plays a crucial role in regulating viral gene expression in EBVaGC.Nucleic acids research · 2023Article
- A distinct isoform of lymphoid enhancer binding factor 1 (LEF1) epigenetically restricts EBV reactivation to maintain viral latency.PLoS pathogens · 2023Article
- Three-Dimensional Chromatin Structure of the EBV Genome: A Crucial Factor in Viral Infection.Viruses · 2023Review
- Reactivation of Epstein-Barr Virus from Latency Involves Increased RNA Polymerase Activity at CTCF Binding Sites on the Viral Genome.Journal of virology · 2023Article
- Dynamics of Viral and Host 3D Genome Structure upon Infection.Journal of microbiology and biotechnology · 2022Review
- Epstein-Barr Virus Viral Processivity Factor EA-D Facilitates Virus Lytic Replication by Inducing Poly(ADP-Ribose) Polymerase 1 Degradation.Journal of virology · 2022Article
- Role of PARP-1 in Human Cytomegalovirus Infection and Functional Partners Encoded by This Virus.Viruses · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The Epstein Barr virus (EBV) genome persists in infected host cells as a chromatinized episome and is subject to chromatin-mediated regulation. Binding of the host insulator protein CTCF to the EBV genome has an established role in maintaining viral latency type, and in other herpesviruses, loss of CTCF binding at specific regions correlates with viral reactivation. Here, we demonstrate that binding of PARP1, an important cofactor of CTCF, at the BZLF1 lytic switch promoter restricts EBV reactivation. Knockdown of PARP1 in the Akata-EBV cell line significantly increases viral copy number and lytic protein expression. Interestingly, CTCF knockdown has no effect on viral reactivation, and CTCF binding across the EBV genome is largely unchanged following reactivation. Moreover, EBV reactivation attenuates PARP activity, and Zta expression alone is sufficient to decrease PARP activity. Here we demonstrate a restrictive function of PARP1 in EBV lytic reactivation.
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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.