ReviewMicroorganisms2019
Epstein-Barr Virus and Innate Immunity: Friends or Foes?
Review in Microorganisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- The role of soluble mediators in the clinical course of EBV infection and B cell homeostasis after kidney transplantation.Scientific reports · 2020Trial
- Integrative Transcriptomics Uncovers IFN-β Signature and IFITM3 as Putative Molecular Mediator in MS.International journal of molecular sciences · 2026Article
- Playing both sides - Epstein-Barr Virus accumulates select cellular transcripts to counter virus-mediated host shut-off in lytic cells.PLoS pathogens · 2026Article
- Single-cell profiling of HDAC inhibitor-induced EBV lytic heterogeneity defines abortive and refractory states in B lymphoblasts.PLoS pathogens · 2026Article
- Molecular mechanisms of Epstein-Barr Virus in the pathogenesis of lymphomas and new opportunities for precision medicine.Discover oncology · 2026Review
- Single-Cell Profiling of HDAC Inhibitor-Induced EBV Lytic Heterogeneity Defines Abortive and Refractory States in B Lymphoblasts.bioRxiv : the preprint server for biology · 2025Article
- SOCS Proteins: Key Players in Immune Regulation During SARS-CoV-2 Infection.European journal of immunology · 2025Review
- Implications of EBV-Encoded and EBV-Related miRNAs in Tumors.Current gene therapy · 2025Review
- HIV-associated cancers and lymphoproliferative disorders caused by Kaposi sarcoma herpesvirus and Epstein-Barr virus.Clinical microbiology reviews · 2024Review
- Serum TLR2 and TLR9 in Prostate Cancer Patients in Relation to EBV Status.International journal of molecular sciences · 2024Article
- Efficacy of NKG2D CAR-T cells with IL-15/IL-15Rα signaling for treating Epstein-Barr virus-associated lymphoproliferative disorder.Experimental hematology & oncology · 2024Article
- Evaluating the role of interleukin-2 and interleukin-12 in pediatric patients with concurrentWorld journal of clinical cases · 2024Article
- Epstein-Barr Viruses: Their Immune Evasion Strategies and Implications for Autoimmune Diseases.International journal of molecular sciences · 2024Review
- Exploring the nuclear proteins, viral capsid protein, and early antigen protein using immunoinformatic and molecular modeling approaches to design a vaccine candidate against Epstein Barr virus.Scientific reports · 2024Article
- Review
- Epstein-Barr virus: the mastermind of immune chaos.Frontiers in immunology · 2024Review
- Article
- Serum and Saliva Level of miR-31-5p and miR-let 7a in EBV Associated Oropharyngeal Cancer.International journal of molecular sciences · 2023Article
- Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of β-Catenin.Microbiology spectrum · 2023Article
- Immunomodulatory Role of Interferons in Viral and Bacterial Infections.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) successfully persists in the vast majority of adults but causes lymphoid and epithelial malignancies in a small fraction of latently infected individuals. Innate immunity is the first-line antiviral defense, which EBV has to evade in favor of its own replication and infection. EBV uses multiple strategies to perturb innate immune signaling pathways activated by Toll-like, RIG-I-like, NOD-like, and AIM2-like receptors as well as cyclic GMP-AMP synthase. EBV also counteracts interferon production and signaling, including TBK1-IRF3 and JAK-STAT pathways. However, activation of innate immunity also triggers pro-inflammatory response and proteolytic cleavage of caspases, both of which exhibit proviral activity under some circumstances. Pathogenic inflammation also contributes to EBV oncogenesis. EBV activates NFκB signaling and induces pro-inflammatory cytokines. Through differential modulation of the proviral and antiviral roles of caspases and other host factors at different stages of infection, EBV usurps cellular programs for death and inflammation to its own benefits. The outcome of EBV infection is governed by a delicate interplay between innate immunity and EBV. A better understanding of this interplay will instruct prevention and intervention of EBV-associated cancers.
Indexed as
Identifiers
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.