ArticleCell host & microbe2017
CRISPR/Cas9 Screens Reveal Epstein-Barr Virus-Transformed B Cell Host Dependency Factors.
Article in Cell host & microbe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
118 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Genome-wide CRISPR screen identifies host dependency factors for influenza A virus infection.Nature communications · 2020Pooled it
- Interferon regulatory factors orchestrate CD8International journal of molecular medicine · 2026Review
- A guide to B cell metabolism.Nature reviews. Immunology · 2026Review
- KSHV-encoded vIRF3 cooperates with cellular IRF4 to drive super-enhancer activity through complex DNA elements.Nucleic acids research · 2026Article
- Arginine metabolism supportsmBio · 2026Article
- Multidimensional analysis of host-virus interactions using the virus-encoded CRISPR-based direct readout system (VECOS).Nature protocols · 2026Review
- CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c.bioRxiv : the preprint server for biology · 2026Article
- Epstein-Barr Virus Latent Membrane Protein 1 Suppresses Ferroptosis via Pentose Phosphate Pathway and Glutathione Metabolism.bioRxiv : the preprint server for biology · 2026Article
- Epstein-Barr Virus Infection at Single-Cell Resolution.Journal of medical virology · 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
- Epstein-barr virus latent membrane protein 1 targets cIAP1, cIAP2 and TRAF2 for proteasomal degradation to activate the non-canonical NF-κB pathway.PLoS pathogens · 2026Article
- Lysine-specific histone demethylase complex restricts Epstein-Barr virus lytic reactivation.Nature microbiology · 2025Article
- The CTLH ubiquitin ligase substrates ZMYND19 and MKLN1 negatively regulate mTORC1 at the lysosomal membrane.Nature communications · 2025Article
- Epstein-Barr virus-transformed B-cells from a hypoxia model of the germinal center requires external unsaturated fatty acids.PLoS pathogens · 2025Article
- Epstein-Barr Virus Encoded lncRNAs Control the Viral Lytic Switch.bioRxiv : the preprint server for biology · 2025Article
- Replication-competent adenovirus reporters utilizing endogenous viral expression architecture.Journal of virology · 2025Article
- Arginine Metabolism SupportsbioRxiv : the preprint server for biology · 2025Article
- Article
- Epstein-Barr Virus Latent Membrane Protein 1 targets cIAP1, cIAP2 and TRAF2 for Proteasomal Degradation to Activate the Non-canonical NF-κB Pathway.bioRxiv : the preprint server for biology · 2025Article
- Insights into absence of lymphoma despite fulminant Epstein-Barr virus infection in patients with XIAP deficiency.JCI insight · 2025Article
58 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
12 authors at 2 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) causes endemic Burkitt lymphoma (BL) and immunosuppression-related lymphomas. These B cell malignancies arise by distinct transformation pathways and have divergent viral and host expression programs. To identify host dependency factors resulting from these EBV+, B cell-transformed cell states, we performed parallel genome-wide CRISPR/Cas9 loss-of-function screens in BL and lymphoblastoid cell lines (LCLs). These highlighted 57 BL and 87 LCL genes uniquely important for their growth and survival. LCL hits were enriched for EBV-induced genes, including viral super-enhancer targets. Our systematic approach uncovered key mechanisms by which EBV oncoproteins activate the PI3K/AKT pathway and evade tumor suppressor responses. LMP1-induced cFLIP was found to be critical for LCL defense against TNFα-mediated programmed cell death, whereas EBV-induced BATF/IRF4 were critical for BIM suppression and MYC induction in LCLs. Finally, EBV super-enhancer-targeted IRF2 protected LCLs against Blimp1-mediated tumor suppression. Our results identify viral transformation-driven synthetic lethal targets for therapeutic intervention.
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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.