ArticleNature microbiology2025
Lysine-specific histone demethylase complex restricts Epstein-Barr virus lytic reactivation.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Proteomic screening identifies HNRNPA2B1 as an epigenetic repressor of Epstein-Barr virus reactivation.Journal of virology · 2026Article
- Arginine metabolism supportsmBio · 2026Article
- Epstein-Barr Virus-host epigenetic interplay: mechanisms of regulation and therapeutic potential.Clinical epigenetics · 2026Review
- SUMOylation and ubiquitination reciprocally regulate SMCHD1 antiviral activity against herpes simplex virus 1.PLoS pathogens · 2026Article
- Locus-specific proteomics identifies novel regulators of Epstein-Barr virus lytic reactivation.Journal of virology · 2026Article
- A CRISPR-Cas9 screen Reveals STEEP1 as a Key Host Dependency Factor for Epstein-Barr Virus Latent Membrane Protein 1 Trafficking and Signaling.bioRxiv : the preprint server for biology · 2026Article
- Proteomic Screening Identifies HNRNPA2B1 as an Epigenetic Repressor of Epstein-Barr Virus Reactivation.bioRxiv : the preprint server for biology · 2026Article
- Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.bioRxiv : the preprint server for biology · 2026Article
- Epstein-Barr virus reactivation triggers selective IL-6/IL-10 axis inflammation and CD3Frontiers in immunology · 2026Article
- Epstein-Barr Virus Encoded lncRNAs Control the Viral Lytic Switch.bioRxiv : the preprint server for biology · 2025Article
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10 authors.
Funding
Abstract
Epstein-Barr virus (EBV) infects >95% of adults and contributes to several human cancers. EBV can remain latent where viral lytic genes are silenced, precluding the use of antiviral agents such as ganciclovir. Little is known about the host factors involved in EBV latency. Here we performed a human genome-wide CRISPR-Cas9 screen in Burkitt lymphoma B cells, which identified lysine-specific histone demethylase 1 (LSD1) and its corepressors REST corepressor 1 (CoREST) and zinc finger protein 217 (ZNF217) as critical for EBV latency. Gene knockout or LSD1 inhibition triggered EBV reactivation, and the latter sensitized cells to ganciclovir cytotoxicity, including in murine tumour xenografts. Mechanistically, ZNF217 recruits LSD1 and CoREST to form a complex that binds a specific DNA motif associated with regions implicated in EBV reactivation. It removes histone 3 lysine 4 (H3K4) methylation marks and restricts host DNA looping. Alternatively, the H3K4 lysine methyltransferase 2D supports EBV lytic reactivation. Our results highlight H3K4 methylation as a major EBV lytic switch regulator and therapeutic target.
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