ArticleJournal of virology2010
Toll-like receptor agonists synergistically increase proliferation and activation of B cells by epstein-barr virus.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 56 citations in OpenAlex.
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- Research landmarks on the 60th anniversary of Epstein-Barr virus.Science China. Life sciences · 2025Review
- Epstein-Barr Viruses: Their Immune Evasion Strategies and Implications for Autoimmune Diseases.International journal of molecular sciences · 2024Review
- Epstein-Barr virus infection: the micro and macro worlds.Virology journal · 2023Review
- Potential role of EBV and Toll-like receptor 9 ligand in patients with systemic lupus erythematosus.Immunologic research · 2023Article
- The role of gastric microecological dysbiosis in gastric carcinogenesis.Frontiers in microbiology · 2023Review
- Anti-viral and pro-inflammatory functions of Toll-like receptors during gamma-herpesvirus infections.Virology journal · 2021Review
- Activation of Innate Immune Responses by a CpG Oligonucleotide Sequence Composed Entirely of Threose Nucleic Acid.Nucleic acid therapeutics · 2019Article
- Herpesviruses: Harmonious Pathogens but Relevant Cofactors in Other Diseases?Frontiers in cellular and infection microbiology · 2018Review
- Epstein-Barr virus microRNAs reduce immune surveillance by virus-specific CD8+ T cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Epstein-Barr viral miRNAs inhibit antiviral CD4+ T cell responses targeting IL-12 and peptide processing.The Journal of experimental medicine · 2016Article
- Characterization of chromatin accessibility with a transposome hypersensitive sites sequencing (THS-seq) assay.Genome biology · 2016Article
- Dysbiotic infection in the stomach.World journal of gastroenterology · 2015Review
- Latent Membrane Protein LMP2A Impairs Recognition of EBV-Infected Cells by CD8+ T Cells.PLoS pathogens · 2015Article
- Plasmodium falciparum infection is associated with Epstein-Barr virus reactivation in pregnant women living in malaria holoendemic area of Western Kenya.Maternal and child health journal · 2015Article
- Article
- Activation of NF-κB via endosomal Toll-like receptor 7 (TLR7) or TLR9 suppresses murine herpesvirus 68 reactivation.Journal of virology · 2014Article
- Assessment of the effect of TLR7/8, TLR9 agonists and CD40 ligand on the transformation efficiency of Epstein-Barr virus in human B lymphocytes by limiting dilution assay.Cytotechnology · 2014Article
- Functional RIG-I-like receptors control the survival of mesenchymal stem cells.Cell death & disease · 2013Article
- Article
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
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV) efficiently drives proliferation of human primary B cells in vitro, a process relevant for human diseases such as infectious mononucleosis and posttransplant lymphoproliferative disease. Human B-cell proliferation is also driven by ligands of Toll-like receptors (TLRs), notably viral or bacterial DNA containing unmethylated CpG dinucleotides, which triggers TLR9. Here we quantitatively investigated how TLR stimuli influence EBV-driven B-cell proliferation and expression of effector molecules. CpG DNA synergistically increased EBV-driven proliferation and transformation, T-cell costimulatory molecules, and early production of interleukin-6. CpG DNA alone activated only memory B cells, but CpG DNA enhanced EBV-mediated transformation of both memory and naive B cells. Ligands for TLR2 or TLR7/8 or whole bacteria had a weaker but still superadditive effect on B-cell transformation. Additionally, CpG DNA facilitated the release of transforming virus by established EBV-infected lymphoblastoid cell lines. These results suggest that the proliferation of EBV-infected B cells and their capability to interact with immune effector cells may be directly influenced by components of bacteria or other microbes present at the site of infection.
Indexed as
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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.