ArticleImmunology2006
Epstein-Barr virus infection negatively impacts the CXCR4-dependent migration of tonsillar B cells.
Article in Immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 26 citations in OpenAlex.
- 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
- Turncoat antibodies unmasked in a model of autoimmune demyelination: From biology to therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comprehensive Bioinformatics Analysis the circRNAs of Viral Infection Associated Pathway in HepG2 Expressing ORF3 of Genotype IV Swine Hepatitis E Virus.Microorganisms · 2025Article
- Observational
- CXCR4 induces cell autophagy and maintains EBV latent infection in EBVaGC.Theranostics · 2020Article
- Role of Epstein-Barr Virus in Pathogenesis and Racial Distribution of IgA Nephropathy.Frontiers in immunology · 2020Article
- Epstein-Barr virus (EBV) provides survival factors to EBVImmunology · 2017Article
- CXCR4: a virus's best friend?Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2014Review
- Cyclooxygenase-2-prostaglandin E2-eicosanoid receptor inflammatory axis: a key player in Kaposi's sarcoma-associated herpes virus associated malignancies.Translational research : the journal of laboratory and clinical medicine · 2013Review
- Concurrent targeting of eicosanoid receptor 1/eicosanoid receptor 4 receptors and COX-2 induces synergistic apoptosis in Kaposi's sarcoma-associated herpesvirus and Epstein-Barr virus associated non-Hodgkin lymphoma cell lines.Translational research : the journal of laboratory and clinical medicine · 2013Article
- C-terminal region of EBNA-2 determines the superior transforming ability of type 1 Epstein-Barr virus by enhanced gene regulation of LMP-1 and CXCR7.PLoS pathogens · 2011Article
- Changes in chemokines and chemokine receptor expression on tonsillar B cells upon Epstein-Barr virus infection.Immunology · 2009Article
- Article
- Epstein-Barr virus (EBV)-infected monocytes facilitate dissemination of EBV within the oral mucosal epithelium.Journal of virology · 2007Article
- EBNA-3B- and EBNA-3C-regulated cellular genes in Epstein-Barr virus-immortalized lymphoblastoid cell lines.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The primary Epstein-Barr virus (EBV) infection occurs in the oropharynx, where the virus infects B cells and subsequently establishes latency in the memory B-cell compartment. EBV has previously been shown to induce changes in the cell surface expression of several chemokine receptors in cell lines and the transfection of EBNA2 or LMP1 into a B-cell-lymphoma-derived cell line decreased the expression of CXCR4. We show that in vitro EBV infection reduces the expression of CXCR4 on primary tonsil B cells already 43 hr after infection. Furthermore, EBV infection affects the chemotactic response to stromal cell-derived factor (SDF-1)alpha/CXCL12, the ligand for CXCR4, with a reduction of SDF-1alpha-induced migration. To clarify whether this reduced migration is EBV-specific or a consequence of cell activation, tonsillar B cells were either infected with EBV, activated with anti-CD40 and interleukin-4 (IL-4) or kept in medium. Activation by anti-CD40 and IL-4 decreased the CXCR4 expression but the CD40 + IL-4-stimulated cells showed no reduction of chemotactic efficacy. Our finding suggests that changing the SDF-1alpha response of the EBV-infected B cells may serve the viral strategy by directing the infected cells into the extrafollicular areas, rather than retaining them in the lymphoepithelium.
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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.