ArticlePLoS pathogens2021
Epigenetic Plasticity Enables CNS-Trafficking of EBV-infected B Lymphocytes.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed.
- From viral epigenetic reprogramming to neuroinflammation: Mechanisms driving neurodegeneration.Journal of neurovirology · 2026Review
- Clinical characteristics of autoimmune GFAP astrocytopathy with concomitant Epstein-Barr virus positivity: a case series of 12 patients and literature review.Journal of neurology · 2026Review
- Latent, Lytic, and Linked to Multiple Sclerosis-How EBV Drives Autoimmunity.European journal of immunology · 2026Review
- Article
- Novel Perspectives Focused on the Relationship Between Herpesvirus Encephalitis and Anti-GFAP-Antibody-Positive Astrocytopathy.Molecular neurobiology · 2025Review
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- The link between gut microbiota and multiple sclerosis from the perspective of barrier function.Frontiers in immunology · 2025Review
- Epstein-Barr virus flare: A multiple sclerosis attack.Surgical neurology international · 2024Review
- Preliminary Study of the Relationship between Osteopontin and Relapsed Hodgkin's Lymphoma.Biomedicines · 2023Article
- The pathogenesis of multiple sclerosis: a series of unfortunate events.Clinical and experimental immunology · 2023Article
- Early autoimmunity and outcome in virus encephalitis: a retrospective study based on tissue-based assay.Journal of neurology, neurosurgery, and psychiatry · 2023Observational
- Inflammation and Epstein-Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection.Viruses · 2023Review
- Epstein-Barr virus as a leading cause of multiple sclerosis: mechanisms and implications.Nature reviews. Neurology · 2023Review
- Comprehensive Investigations Relationship Between Viral Infections and Multiple Sclerosis Pathogenesis.Current microbiology · 2022Review
- Exploring epigenetic reprogramming during central nervous system infection.Immunological reviews · 2022Review
- B cells going viral in the CNS: Dynamics, complexities, and functions of B cells responding to viral encephalitis.Immunological reviews · 2022Review
- Altered Immune Response to the Epstein-Barr Virus as a Prerequisite for Multiple Sclerosis.Cells · 2022Review
- CD4+ Cytotoxic T Cells Involved in the Development of EBV-Associated Diseases.Pathogens (Basel, Switzerland) · 2022Review
- What do animal models tell us about the role of EBV in the pathogenesis of multiple sclerosis?Frontiers in immunology · 2022Review
- Primary Peripheral Epstein-Barr Virus Infection Can Lead to CNS Infection and Neuroinflammation in a Rabbit Model: Implications for Multiple Sclerosis Pathogenesis.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Subpopulations of B-lymphocytes traffic to different sites and organs to provide diverse and tissue-specific functions. Here, we provide evidence that epigenetic differences confer a neuroinvasive phenotype. An EBV+ B cell lymphoma cell line (M14) with low frequency trafficking to the CNS was neuroadapted to generate a highly neuroinvasive B-cell population (MUN14). MUN14 B cells efficiently infiltrated the CNS within one week and produced neurological pathologies. We compared the gene expression profiles of viral and cellular genes using RNA-Seq and identified one viral (EBNA1) and several cellular gene candidates, including secreted phosphoprotein 1/osteopontin (SPP1/OPN), neuron navigator 3 (NAV3), CXCR4, and germinal center-associated signaling and motility protein (GCSAM) that were selectively upregulated in MUN14. ATAC-Seq and ChIP-qPCR revealed that these gene expression changes correlated with epigenetic changes at gene regulatory elements. The neuroinvasive phenotype could be attenuated with a neutralizing antibody to OPN, confirming the functional role of this protein in trafficking EBV+ B cells to the CNS. These studies indicate that B-cell trafficking to the CNS can be acquired by epigenetic adaptations and provide a new model to study B-cell neuroinvasion associated CNS lymphoma and autoimmune disease of the CNS, including multiple sclerosis (MS).
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