ArticlemBio2021
The Epstein-Barr Virus Oncogene EBNA1 Suppresses Natural Killer Cell Responses and Apoptosis Early after Infection of Peripheral B Cells.
Article in mBio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 39 citations in OpenAlex.
- Multiple Sclerosis and Viruses: « Liaisons Dangereuses ».Reviews in medical virology · 2026Review
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- Association of EBV EBNA1 C-terminal variations with severity of Invasive ductal carcinoma.Molecular biology reports · 2026Article
- EBV hijacks the metabolic function of CD73 to resist the antitumor function of NK cells.NPJ precision oncology · 2026Article
- Epstein-Barr Virus-Mediated Apoptosis Evasion in Epithelial Malignancies: Molecular Mechanisms and Therapeutic Implications.Biology · 2026Review
- Targeted Epstein-Barr virus capture sequencing identifies BBLF4-L322M as an independent prognostic variant in nasopharyngeal carcinoma.Microbiology spectrum · 2026Article
- Research progress on the mechanisms of EB virus reshaping the immune microenvironment in nasopharyngeal carcinoma.Clinical and experimental medicine · 2026Review
- Epacadostat and Olaparib Synergistically Inhibit the Growth of BRCA-Proficient Triple-Negative Breast Cancer by Suppressing the Expression of BRCA1 and RAD51.Molecules (Basel, Switzerland) · 2026Article
- The immunosuppressive tumor microenvironment in post-transplant lymphoproliferative disorder: pathogenesis and novel therapeutic frontiers.Frontiers in immunology · 2026Review
- The role of Epstein-Barr virus in NK/T cell lymphoproliferative disorders: molecular mechanisms and potential therapeutic strategies.Frontiers in immunology · 2026Review
- Epstein-Barr virus: biology, pathogenesis and therapy of lymphomas.Discover oncology · 2025Review
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Review
- Virus-mediated immunosuppression in head and neck cancer.Oncogene · 2025Review
- [Multiple sclerosis and the Epstein-Barr Virus: Current perspectives on their pathogenic mechanisms].Revista medica del Instituto Mexicano del Seguro Social · 2025Review
- Genetic evidence identifies a causal relationship between EBV infection and multiple myeloma risk.Scientific reports · 2025Article
- How Epstein Barr Virus Causes Lymphomas.Viruses · 2024Review
- Carcinogenic mechanisms of virus-associated lymphoma.Frontiers in immunology · 2024Review
- Epstein-Barr virus: the mastermind of immune chaos.Frontiers in immunology · 2024Review
- Epstein-Barr virus infection: the micro and macro worlds.Virology journal · 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
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The innate immune system serves as frontline defense against pathogens, such as bacteria and viruses. Natural killer (NK) cells are a part of innate immunity and can both secrete cytokines and directly target cells for lysis. NK cells express several cell surface receptors, including NKG2D, which bind multiple ligands. People with deficiencies in NK cells are often susceptible to uncontrolled infection by herpesviruses, such as Epstein-Barr virus (EBV). Infection with EBV stimulates both innate and adaptive immunity, yet the virus establishes lifelong latent infection in memory B cells. We show that the EBV oncogene EBNA1, previously known to be necessary for maintaining EBV genomes in latently infected cells, also plays an important role in suppressing NK cell responses and cell death in newly infected cells. EBNA1 does so by downregulating the NKG2D ligands ULBP1 and ULBP5 and modulating expression of c-Myc. B cells infected with a derivative of EBV that lacks EBNA1 are more susceptible to NK cell-mediated killing and show increased levels of apoptosis. Thus, EBNA1 performs a previously unappreciated role in reducing immune response and programmed cell death after EBV infection, helping infected cells avoid immune surveillance and apoptosis and thus persist for the lifetime of the host.
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.