ArticleJournal of virology2013
Signal transducer and activator of transcription 3 limits Epstein-Barr virus lytic activation in B lymphocytes.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 53 citations in OpenAlex.
- Playing both sides - Epstein-Barr Virus accumulates select cellular transcripts to counter virus-mediated host shut-off in lytic cells.PLoS pathogens · 2026Article
- Single-cell profiling of HDAC inhibitor-induced EBV lytic heterogeneity defines abortive and refractory states in B lymphoblasts.PLoS pathogens · 2026Article
- Epstein-Barr Virus Encoded lncRNAs Control the Viral Lytic Switch.bioRxiv : the preprint server for biology · 2025Article
- Single-Cell Profiling of HDAC Inhibitor-Induced EBV Lytic Heterogeneity Defines Abortive and Refractory States in B Lymphoblasts.bioRxiv : the preprint server for biology · 2025Article
- Review
- STAT3, MYC, and EBNA1 cooperate through a ZC3H18 transcriptional network to regulate survival and proliferation of EBV-positive lymphomas.PLoS pathogens · 2025Article
- KAP1/TRIM28 - antiviral and proviral protagonist of herpesvirus biology.Trends in microbiology · 2024Article
- Curcumin derivative C210 induces Epstein-Barr virus lytic cycle and inhibits virion production by disrupting Hsp90 function.Scientific reports · 2024Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.PLoS pathogens · 2024Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.bioRxiv : the preprint server for biology · 2024Article
- Germinal center cytokine driven epigenetic control of Epstein-Barr virus latency gene expression.PLoS pathogens · 2024Article
- Latent Epstein-Barr virus infection collaborates with Myc over-expression in normal human B cells to induce Burkitt-like Lymphomas in mice.PLoS pathogens · 2024Article
- Reactivation of Epstein-Barr Virus from Latency Involves Increased RNA Polymerase Activity at CTCF Binding Sites on the Viral Genome.Journal of virology · 2023Article
- SARS-CoV-2 infection and lytic reactivation of herpesviruses: A potential threat in the postpandemic era?Journal of medical virology · 2022Review
- IFI16 Partners with KAP1 to Maintain Epstein-Barr Virus Latency.Journal of virology · 2022Article
- The Anti-COVID-19 Drug Remdesivir Promotes Oncogenic Herpesvirus Reactivation through Regulation of Intracellular Signaling Pathways.Antimicrobial agents and chemotherapy · 2022Article
- Prazoles Targeting Tsg101 Inhibit Release of Epstein-Barr Virus following Reactivation from Latency.Journal of virology · 2021Article
- Inflammasome, the Constitutive Heterochromatin Machinery, and Replication of an Oncogenic Herpesvirus.Viruses · 2021Review
- A heterochromatin inducing protein differentially recognizes self versus foreign genomes.PLoS pathogens · 2021Article
- An Ancestral Retrovirus Envelope Protein Regulates Persistent Gammaherpesvirus Lifecycles.Frontiers in microbiology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 3 countries.
Funding
Abstract
Lytic activation of Epstein-Barr virus (EBV) is central to its life cycle and to most EBV-related diseases. However, not every EBV-infected B cell is susceptible to lytic activation. This lack of uniform susceptibility to lytic activation also directly impacts the success of viral oncolytic therapy for EBV cancers, yet determinants of susceptibility to lytic induction signals are not well understood. To determine if host factors influence susceptibility to EBV lytic activation, we developed a technique to separate lytic from refractory cells and reported that EBV lytic activation occurs preferentially in cells with lower levels of signal transducer and activator of transcription 3 (STAT3). Using this tool to detect single cells, we now extend the correlation between STAT3 and lytic versus refractory states to EBV-infected circulating B cells in patients with primary EBV infection, leading us to investigate whether STAT3 controls susceptibility to EBV lytic activation. In loss-of-function and gain-of-function studies in EBV-positive B lymphoma and lymphoblastoid cells, we found that the levels of functional STAT3 regulate susceptibility to EBV lytic activation. This prompted us to identify a pool of candidate cellular genes that might be regulated by STAT3 to limit EBV lytic activation. From this pool, we confirmed increases in transcript levels in refractory cells of a set of genes known to participate in transcription repression. Taken together, our findings place STAT3 at a critical crossroads between EBV latency and lytic activation, processes fundamental to EBV lymphomagenesis.
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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.