ArticlePloS one2015
IL6 Inhibits HBV Transcription by Targeting the Epigenetic Control of the Nuclear cccDNA Minichromosome.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers, 1 of them a synthesis that pooled it.
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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.
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, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Risk of Reactivation of Hepatitis B Virus (HBV) and Tuberculosis (TB) and Complications of Hepatitis C Virus (HCV) Following Tocilizumab Therapy: A Systematic Review to Inform Risk Assessment in the COVID-19 Era.Frontiers in medicine · 2021Pooled it
- Circulating and intrahepatic antiviral B cells are defective in hepatitis B.The Journal of clinical investigation · 2018Trial
- Exploring the partial immunological mechanisms of hepatitis B virus reactivation in patients with hepatitis B and tuberculosis.Frontiers in cellular and infection microbiology · 2026Article
- Reduced HBsAg positivity in systemic lupus erythematosus and Sjögren's syndrome: A retrospective comparative study.Biochemistry and biophysics reports · 2025Article
- [Research progress on B cells in chronic hepatitis B].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025Review
- HBV cccDNA: The Molecular Reservoir of Hepatitis B Persistence and Challenges to Achieve Viral Eradication.Biomolecules · 2025Review
- Hepatitis B virus evades the immune system by suppressing the NF-κB signaling pathway with DENND2A.Microbiology spectrum · 2024Article
- Dysfunction and regulatory interplay of T and B cells in chronic hepatitis B: immunotherapy and emerging antiviral strategies.Frontiers in cellular and infection microbiology · 2024Review
- Nuclear RPSA senses viral nucleic acids to promote the innate inflammatory response.Nature communications · 2023Article
- The role of HBV cccDNA in occult hepatitis B virus infection.Molecular and cellular biochemistry · 2023Review
- [Regulation and influence of mitochondria on macrophages during hepatitis B virus infection].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Article
- Article
- Screening of an epigenetic compound library identifies BRD4 as a potential antiviral target for hepatitis B virus covalently closed circular DNA transcription.Antiviral research · 2023Article
- Reviewing the Potential Links between Viral Infections and TDP-43 Proteinopathies.International journal of molecular sciences · 2023Review
- Inhibition of Hepatitis B Virus (HBV) replication and antigen expression byFrontiers in cellular and infection microbiology · 2023Article
- Inducers of the NF-κB pathways impair hepatitis delta virus replication and strongly decrease progeny infectivityJHEP reports : innovation in hepatology · 2022Article
- Innate and Adaptive Immunopathogeneses in Viral Hepatitis; Crucial Determinants of Hepatocellular Carcinoma.Cancers · 2022Review
- Hepatocytes: A key role in liver inflammation.Frontiers in immunology · 2022Review
- Characterization of a KDM5 small molecule inhibitor with antiviral activity against hepatitis B virus.PloS one · 2022Article
- Efficient cellular and humoral immune response and production of virus-neutralizing antibodies by the Hepatitis B Virus S/preS1Frontiers in immunology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The HBV covalently closed circular DNA (cccDNA) is organized as a mini-chromosome in the nuclei of infected hepatocytes by histone and non-histone proteins. Transcription from the cccDNA of the RNA replicative intermediate termed pre-genome (pgRNA), is the critical step for genome amplification and ultimately determines the rate of HBV replication. Multiple evidences suggest that cccDNA epigenetic modifications, such as histone modifications and DNA methylation, participate in regulating the transcriptional activity of the HBV cccDNA. Inflammatory cytokines (TNFα, LTβ) and the pleiotropic cytokine interleukin-6 (IL6) inhibit hepatitis B virus (HBV) replication and transcription. Here we show, in HepG2 cells transfected with linear HBV monomers and HBV-infected NTCP-HepG2 cells, that IL6 treatment leads to a reduction of cccDNA-bound histone acetylation paralleled by a rapid decrease in 3.5kb/pgRNA and subgenomic HBV RNAs transcription without affecting cccDNA chromatinization or cccDNA levels. IL6 repressive effect on HBV replication is mediated by a loss of HNF1α and HNF4α binding to the cccDNA and a redistribution of STAT3 binding from the cccDNA to IL6 cellular target genes.
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