ArticleProceedings of the National Academy of Sciences of the United States of America2016
Mouse model for acute Epstein-Barr virus infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Review
- 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 targets cIAP1, cIAP2 and TRAF2 for proteasomal degradation to activate the non-canonical NF-κB pathway.PLoS pathogens · 2026Article
- 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
- Epstein-Barr virus latent membrane protein 1 subverts IMPDH pathways to drive B-cell oncometabolism.PLoS pathogens · 2025Article
- T cell-mediated immune surveillance conferred by latent Epstein-Barr virus genes suppresses a broad spectrum of tumor formation through NKG2D-NKG2DL interactions.Frontiers in immunology · 2025Article
- Co-expression of PD1+ and HLA-DR+ in CD8+ T cells is increased in tonsils of children with EBV primary and persistent infection.Frontiers in immunology · 2025Article
- Expansion and Precise CRISPR-Cas9 Gene Repair of Autologous T-Memory Stem Cells from Patients with T-Cell Immunodeficiencies.Bio-protocol · 2024Article
- Roles and regulation of microglia activity in multiple sclerosis: insights from animal models.Nature reviews. Neuroscience · 2023Review
- LMP1 mediates tumorigenesis through persistent epigenetic modifications and PGC1β upregulation.Oncology reports · 2023Article
- Concomitant Cytotoxic Effector Differentiation of CD4Cancers · 2022Article
- Latent gammaherpesvirus exacerbates arthritis through modification of age-associated B cells.eLife · 2021Article
- Pathologically Relevant Mouse Models for Epstein-Barr Virus-Associated B Cell Lymphoma.Frontiers in immunology · 2021Review
- Gender and the Sex Hormone Estradiol Affect Multiple Sclerosis Risk Gene Expression in Epstein-Barr Virus-Infected B Cells.Frontiers in immunology · 2021Article
- Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell lymphomagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Differences in Epstein-Barr Virus Characteristics and Viral-Related Microenvironment Could Be Responsible for Lymphomagenesis in Children.Pathogens (Basel, Switzerland) · 2020Article
- Mechanisms of B-Cell Oncogenesis Induced by Epstein-Barr Virus.Journal of virology · 2019Review
- Epigenetic crossroads of the Epstein-Barr virus B-cell relationship.Current opinion in virology · 2018Review
- Co-Expression of the Epstein-Barr Virus-Encoded Latent Membrane Proteins and the Pathogenesis of Classic Hodgkin Lymphoma.Cancers · 2018Review
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr Virus (EBV) infects human B cells and drives them into continuous proliferation. Two key viral factors in this process are the latent membrane proteins LMP1 and LMP2A, which mimic constitutively activated CD40 receptor and B-cell receptor signaling, respectively. EBV-infected B cells elicit a powerful T-cell response that clears the infected B cells and leads to life-long immunity. Insufficient immune surveillance of EBV-infected B cells causes life-threatening lymphoproliferative disorders, including mostly germinal center (GC)-derived B-cell lymphomas. We have modeled acute EBV infection of naive and GC B cells in mice through timed expression of LMP1 and LMP2A. Although lethal when induced in all B cells, induction of LMP1 and LMP2A in just a small fraction of naive B cells initiated a phase of rapid B-cell expansion followed by a proliferative T-cell response, clearing the LMP-expressing B cells. Interfering with T-cell activity prevented clearance of LMP-expressing B cells. This was also true for perforin deficiency, which in the human causes a life-threatening EBV-related immunoproliferative syndrome. LMP expression in GC B cells impeded the GC reaction but, upon loss of T-cell surveillance, led to fatal B-cell expansion. Thus, timed expression of LMP1 together with LMP2A in subsets of mouse B cells allows one to study major clinically relevant features of human EBV infection in vivo, opening the way to new therapeutic approaches.
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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.