ArticleProceedings of the National Academy of Sciences of the United States of America2005
Peripheral B cells latently infected with Epstein-Barr virus display molecular hallmarks of classical antigen-selected memory B cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- Steroids for symptom control in infectious mononucleosis.The Cochrane database of systematic reviews · 2015Pooled it
- Viral subversion of B-cell tolerance: mechanisms linking infection to autoimmunity.EMBO reports · 2026Review
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- SIRT2 deacylase modulators control B cell metabolic reprogramming in EBV infection and mitogenic activation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A tonsil organoid model reveals Epstein-Barr virus-infected germinal center B cell states during primary infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- What would it take to prove that a chronic infection is a causal agent in Alzheimer's disease?Trends in neurosciences · 2025Review
- Oral hairy leukoplakia: The role of Epstein-Barr virus, the occurrence in immunocompetent patients, and the malignant transformation potential.Journal of dental sciences · 2025Review
- Fatty acid desaturases link cell metabolism pathways to promote proliferation of Epstein-Barr virus-infected B cells.PLoS pathogens · 2025Article
- A thorough insight into the life cycle of the Epstein-Barr virus. From the molecular to the organismal level.Current research in microbial sciences · 2025Review
- Epstein-Barr virus and host cell 3D genome organization.Journal of medical virology · 2023Review
- Spontaneous EBV-Reactivation during B Cell Differentiation as a Model for Polymorphic EBV-Driven Lymphoproliferation.Cancers · 2023Article
- A Review of Compartmentalised Inflammation and Tertiary Lymphoid Structures in the Pathophysiology of Multiple Sclerosis.Biomedicines · 2022Review
- Review
- Immune Control ofViral immunology · 2020Article
- Gammaherpesvirus Colonization of the Spleen Requires Lytic Replication in B Cells.Journal of virology · 2018Article
- Epstein-Barr virus nuclear antigen EBNA-LP is essential for transforming naïve B cells, and facilitates recruitment of transcription factors to the viral genome.PLoS pathogens · 2018Article
- Deciphering the Role of B Cells in Multiple Sclerosis-Towards Specific Targeting of Pathogenic Function.International journal of molecular sciences · 2017Review
- Evidence for a Mesothelial Origin of Body Cavity Effusion Lymphomas.Journal of the National Cancer Institute · 2017Article
- Impact of Chronic Viral Infection on T-Cell Dependent Humoral Immune Response.Frontiers in immunology · 2017Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) establishes a lifelong persistent infection within peripheral blood B cells with the surface phenotype of memory cells. To date there is no proof that these cells have the genotype of true germinal-center-derived memory B cells. It is critical to understand the relative contribution of viral mimicry versus antigen signaling to the production of these cells because EBV encodes proteins that can affect the surface phenotype of infected cells and provide both T cell help and B cell receptor signals in the absence of cognate antigen. To address these questions we have developed a technique to identify single EBV-infected cells in the peripheral blood and examine their expressed Ig genes. The genes were all isotype-switched and somatically mutated. Furthermore, the mutations do not cause stop codons and display the pattern expected for antigen-selected memory cells based on their frequency, type, and location within the Ig gene. We conclude that latently infected peripheral blood B cells display the molecular hallmarks of classical antigen-selected memory B cells. Therefore, EBV does not disrupt the normal processing of latently infected cells into memory, and deviations from normal B cell biology are not tolerated in the infected cells. This article provides definitive evidence that EBV in the peripheral blood persists in true memory B cells.
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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.