ArticleNAR cancer2025
Leveraging the interconnected unfolded protein response and NLRP3 inflammasome pathways to reactivate Epstein-Barr virus in diffuse large B-cell lymphomas.
Article in NAR cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- RSAD2/VIPERIN and CMPK2 coordinate an immunometabolic response to Epstein-Barr Virus.PLoS pathogens · 2026Article
- Arginine metabolism supportsmBio · 2026Article
- 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
- Immune escape mechanisms and therapeutic advances in virus-associated hematological malignancies.Blood cancer journal · 2026Review
- RSAD2/VIPERIN and CMPK2 Coordinate an Immunometabolic Response to Epstein-Barr Virus.bioRxiv : the preprint server for biology · 2026Article
- Arginine Metabolism SupportsbioRxiv : 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
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Authors and funding
7 authors.
Funding
Abstract
Diffuse large B-cell lymphoma (DLBCL), when associated with Epstein-Barr virus (EBV) in immunocompromised individuals such as AIDS patients, presents a significant treatment challenge. Lytic induction therapy, which reactivates latent EBV to directly kill tumor cells and sensitize them to nucleoside analogs that block viral replication and immune clearance, offers promise. However, little is known about EBV reactivation in DLBCL. Here, we examined four EBV-positive DLBCL cell lines and found variable, cell-line-specific responses to lytic stimuli, with most showing an abortive response-either before or after genome replication, without virus release. This is in contrast to commonly studied lymphoma cells in which EBV reactivation typically leads to a full lytic cycle. Mechanistically, we show that the unfolded protein response (UPR), via a splice variant of the transcription factor XBP1, upregulates TXNIP and NLRP3, activating the inflammasome and removing a barrier to transcription of the EBV latent-to-lytic switch gene
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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.