ArticleJournal of virology2003
Tumor necrosis factor alpha inhibition of hepatitis B virus replication involves disruption of capsid Integrity through activation of NF-kappaB.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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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.
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Who cites it
71 citing papers in PubMed, 164 citations in OpenAlex.
- Sci-B-VacTM Vs ENGERIX-B Vaccines for Hepatitis B Virus in Patients with Inflammatory Bowel Diseases: A Randomised Controlled Trial.Journal of Crohn's & colitis · 2016Trial
- A Quantitative Systems Pharmacology (QSP) Model of Acute Hepatitis B Virus Infection: Mechanistic Insights and Foundations for Future Extensions.CPT: pharmacometrics & systems pharmacology · 2026Article
- Contradictory Mechanisms of rheumatoid arthritis and hepatitis B virus infection activation.Heliyon · 2025Review
- M1/M2 macrophages and their overlaps - myth or reality?Clinical science (London, England : 1979) · 2023Article
- System Biology Investigation Revealed Lipopolysaccharide and Alcohol-Induced Hepatocellular Carcinoma Resembled Hepatitis B Virus Immunobiology and Pathogenesis.International journal of molecular sciences · 2023Article
- Mesenchymal stem cells-based therapy in liver diseases.Molecular biomedicine · 2022Review
- TNF in the liver: targeting a central player in inflammation.Seminars in immunopathology · 2022Review
- Efficient cellular and humoral immune response and production of virus-neutralizing antibodies by the Hepatitis B Virus S/preS1Frontiers in immunology · 2022Article
- Host Factors in the Natural History of Chronic Hepatitis B: Role of Genetic Determinants.International journal of hepatology · 2022Article
- Hepatitis B virus middle surface antigen loss promotes clinical variant persistence in mouse models.Virulence · 2021Article
- Elevated NTCP expression by an iPSC-derived human hepatocyte maintenance medium enhances HBV infection in NTCP-reconstituted HepG2 cells.Cell & bioscience · 2021Article
- Immunopathology of Chronic Hepatitis B Infection: Role of Innate and Adaptive Immune Response in Disease Progression.International journal of molecular sciences · 2021Review
- The Potential Role of Probiotics in Protection against Influenza a Virus Infection in Mice.Foods (Basel, Switzerland) · 2021Article
- Article
- Hepatitis B Virus Induces Autophagy to Promote its Replication by the Axis of miR-192-3p-XIAP Through NF kappa B Signaling.Hepatology (Baltimore, Md.) · 2019Article
- Intracellular interleukin-32γ mediates antiviral activity of cytokines against hepatitis B virus.Nature communications · 2018Article
- Tumor necrosis factor: The key to hepatitis B viral clearance.Cellular & molecular immunology · 2018Article
- HBV-Derived Synthetic Long Peptide Can Boost CD4+ and CD8+ T-Cell Responses in Chronic HBV Patients Ex Vivo.The Journal of infectious diseases · 2018Article
- B-Cell Lymphoma 6 (BCL6) Is a Host Restriction Factor That Can Suppress HBV Gene Expression and Modulate Immune Responses.Frontiers in microbiology · 2018Article
- Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Chronic infection by hepatitis B virus results from an inability to clear the virus, which is associated with liver disease and liver cancer. Tumor necrosis factor alpha (TNF-alpha) is associated with noncytopathic clearance of hepatitis B virus in animal models. Here we demonstrate that the nuclear factor kappaB (NF-kappaB) signaling pathway is a central mediator of inhibition of hepatitis B virus by TNF-alpha and we describe the molecular mechanism. TNF-alpha is shown to suppress hepatitis B virus DNA replication without cell killing by disrupting the formation or stability of cytoplasmic viral capsids through a pathway requiring the NF-kappaB-activating inhibitor of kappaB kinase complex IKK-alpha/beta and active transcription factor NF-kappaB. Hepatitis B virus replication could also be inhibited and viral capsid formation could be disrupted in the absence of TNF-alpha solely by overexpression of IKK-alpha/beta or strong activation of NF-kappaB. In contrast, inhibition of NF-kappaB signaling stimulated viral replication, demonstrating that HBV replication is both positively and negatively regulated by the level of activity of the NF-kappaB pathway. Studies are presented that exclude the possibility that HBV inhibition by NF-kappaB is carried out by secondary production of gamma interferon or alpha/beta interferon. These results identify a novel mechanism for noncytopathic suppression of hepatitis B virus replication that is mediated by the NF-kappaB signaling pathway and activated by TNF-alpha.
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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.