ReviewCurrent topics in microbiology and immunology2015
EBV Persistence--Introducing the Virus.
Review in Current topics in microbiology and immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers.
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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
229 citing papers in PubMed, 336 citations in OpenAlex.
- Multiple Sclerosis and Viruses: « Liaisons Dangereuses ».Reviews in medical virology · 2026Review
- CD20 bispecific T-cell engager depletes B-cell progenitors preventing EBV-associated lymphomagenesis in humanized mice.Blood advances · 2026Article
- Next-generation LMP2A-targeting TCR-recombinant T cells with inducible IL-18 expression to treat EBV-associated malignancies.Molecular therapy. Oncology · 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
- The ageing immune system and its battle with viruses.The Journal of general virology · 2026Review
- Immunological Determinants of Oncogenic Virus-Driven Cancers in Africa: Mechanisms, Co-Infections and Public Health Challenges.Pathogens (Basel, Switzerland) · 2026Review
- Review
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- The Microbiome-Mitochondria-Extracellular Vesicle Axis in HPV Persistence and Cervical Carcinogenesis.Genes · 2026Review
- Cellular Metabolic Signatures of Long COVID-19.Infectious disease reports · 2026Article
- Article
- Observational
- Article
- Molecular mechanisms of Epstein-Barr Virus in the pathogenesis of lymphomas and new opportunities for precision medicine.Discover oncology · 2026Review
- Increased Frequency of the Chemokine Receptor CCR2 on Circulating CD19+CD5+ Lymphocytes in Therapy-Naïve CLL Patients With the Detectable EBV DNA and High-Avidity Antibodies Against the EBV Capsid Antigen.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026Article
- IgA nephropathy: a novel pathway in immunopathogenesis dependent on the timing of Epstein-Barr virus infection.Frontiers in immunology · 2026Review
- Hit-and-run hypothesis: revisiting the impact of EBV in malignancies.Frontiers in immunology · 2026Review
- Relationship between Epstein-Barr virus and inflammatory bowel disease.World journal of gastroenterology · 2025Review
- Lysine-specific histone demethylase complex restricts Epstein-Barr virus lytic reactivation.Nature microbiology · 2025Article
- Human Cytomegalovirus and Epstein-Barr Virus Infection in Inflammatory Bowel Disease: Crossing the Diagnostic Barrier for Appropriate Management.Biomedicines · 2025Article
169 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Persistent infection by EBV is explained by the germinal center model (GCM) which provides a satisfying and currently the only explanation for EBVs disparate biology. Since the GCM touches on every aspect of the virus, this chapter will serve as an introduction to the subsequent chapters. EBV is B lymphotropic, and its biology closely follows that of normal mature B lymphocytes. The virus persists quiescently in resting memory B cells for the lifetime of the host in a non-pathogenic state that is also invisible to the immune response. To access this compartment, the virus infects naïve B cells in the lymphoepithelium of the tonsils and activates these cells using the growth transcription program. These cells migrate to the GC where they switch to a more limited transcription program, the default program, which helps rescue them into the memory compartment where the virus persists. For egress, the infected memory cells return to the lymphoepithelium where they occasionally differentiate into plasma cells activating viral replication. The released virus can either infect more naïve B cells or be amplified in the epithelium for shedding. This cycle of infection and the quiescent state in memory B cells allow for lifetime persistence at a very low level that is remarkably stable over time. Mathematically, this is a stable fixed point where the mechanisms regulating persistence drive the state back to equilibrium when perturbed. This is the GCM of EBV persistence. Other possible sites and mechanisms of persistence will also be discussed.
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What OpenQuestion holds
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.