ArticleNature communications2025
Epstein-Barr virus induces aberrant B cell migration and diapedesis via FAK-dependent chemotaxis pathways.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Epstein-Barr virus (EBV) infection causes human germinal center B cell-derived lymphomas in the absence of EBNA2 expression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Increased Expression of CXCL9, CXCL10, and CXCL11 in Epstein-Barr Virus-Associated Infectious Mononucleosis and the Role of CXCL5 as a Candidate Biomarker of Disease Severity.Pathogens (Basel, Switzerland) · 2026Article
- Development of a Diagnostic Autoantibody Assay to a Consensus Motif for the Risk Prediction of Epstein-Barr Virus-Related Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Neuroinflammation as a result of non-neurotropic herpesvirus infection.Immunology and cell biology · 2026Review
- Epstein-Barr Virus Infection at Single-Cell Resolution.Journal of medical virology · 2026Review
- Epstein-Barr virus reactivation triggers selective IL-6/IL-10 axis inflammation and CD3Frontiers in immunology · 2026Article
- Epstein-Barr virus and spontaneous lymphoblastoid cell lines: establishment, molecular characteristics, immune modulation, and therapeutic insight.Clinical and experimental immunology · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Infection with the Epstein-Barr virus (EBV) is a major risk factor for the development of cancer and autoimmune disorders. The virus enters the body in the pharynx, but EBV causes disease in distant organs, including the gut and the brain. Here we show, using in vitro culture and mouse infection models, that EBV-infected B cells display features of homing cells. Infected B cells undergo migration following paracrine CCL4 release and CCR1 induction, while CCR1 deficiency inhibits migration and, unexpectedly, proliferation of infected B cells. Furthermore, migrating EBV-infected B cells undergo CCL4-dependent diapedesis, induce ICAM-1 on endothelial cells, and disrupt the integrity of endothelial barriers. Both migration and diapedesis are regulated by FAK, with FAK inhibition blocking growth and survival of EBV-transformed B cells, as well as their spreading to spleen and brain in an animal model in vivo. Moreover, IL-10 secreted by EBV-infected B cells attracts and facilitates diapedesis of EBV-negative CD52
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Registered trials
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