ArticleScience (New York, N.Y.)2014
Specific and nonhepatotoxic degradation of nuclear hepatitis B virus cccDNA.
Article in Science (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 487 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
487 citing papers in PubMed, 862 citations in OpenAlex.
- Predictive model for HBsAg clearance rate in chronic hepatitis B patients treated with pegylated interferon α-2b for 48 weeks.Hepatology international · 2025Trial
- pgRNA-mEpigenetics · 2026Article
- Viral persistence and immune dysfunction in chronic hepatitis B: Mechanisms of post-treatment antigen asynchrony.iScience · 2026Review
- Discontinuation of nucleos(t)ide analog therapy in hepatitis B e antigen-negative non-cirrhotic chronic hepatitis B patients: A real-life study.World journal of virology · 2026Article
- Hepatitis B Virus: Epidemiology, Prophylaxis, Therapy, Clinical Outcomes, and Novel Therapeutic Directions.Biomolecules · 2026Review
- Review
- Core protein mutations are key determinants of hepatitis B virus replication during the hepatitis B e antigen-negative stage.The Journal of general virology · 2026Article
- Review
- Persistent loss of intrahepatic IFN-γ in HBV is linked to selective impairment of liver-resident CXCR6+NK cells despite long-term NUC therapy.JHEP reports : innovation in hepatology · 2026Article
- The NF-κB Signalling Pathway: Mechanisms, Consequences and Therapeutic Targets.Journal of cellular and molecular medicine · 2026Review
- Reconsidering the role of plasma pgRNA in NUC-treated CHB: Stratified biomarker interpretation and the limits of current assays: Letter to the editor on "Longitudinal profile of plasma pregenomic RNA in patients with chronic hepatitis B infection on long-term nucleoside analogues and its interaction with clinical parameters".Clinical and molecular hepatology · 2026Article
- IFI35 suppresses the transcription of hepatitis B virus cccDNA minichromosome via promoting HNF4α proteasomal degradation.Journal of biomedical science · 2026Article
- hnRNPA2B1 induces HBV cccDNA degradation by recruiting APOBEC3B.Nucleic acids research · 2026Article
- Identification of Marine-Derived Compounds with Potent Antiviral Activity in a Recombinant HBV cccDNA Cell Model.ACS omega · 2026Article
- Hepatocyte-Targeted Drug Delivery Strategies for Chronic Hepatitis B: Overcoming Delivery Barriers Toward Functional Cure.Pharmaceutics · 2026Review
- Insight into the Biology of Hepatitis B Virus and Recent Therapeutic Approaches.Current microbiology · 2026Review
- Functional immune responses induced by a capsid assembly modulator in chronic hepatitis B virus-infected humanized mice.Cell host & microbe · 2026Article
- PYHIN proteins: guardians or contributors to hepatitis B virus pathogenesis?Frontiers in immunology · 2026Review
- Innate immune recognition and evasion strategies of hepatitis B virus: from DNA to RNA and viral proteins.Frontiers in immunology · 2026Review
- The central regulator HIF-1α in digestive system pathologies: inflammation and cancer.Frontiers in immunology · 2026Review
427 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
- Commented on by
- Commented on by
Authors and funding
24 authors at 4 institutions in 3 countries.
Funding
Abstract
Current antiviral agents can control but not eliminate hepatitis B virus (HBV), because HBV establishes a stable nuclear covalently closed circular DNA (cccDNA). Interferon-α treatment can clear HBV but is limited by systemic side effects. We describe how interferon-α can induce specific degradation of the nuclear viral DNA without hepatotoxicity and propose lymphotoxin-β receptor activation as a therapeutic alternative. Interferon-α and lymphotoxin-β receptor activation up-regulated APOBEC3A and APOBEC3B cytidine deaminases, respectively, in HBV-infected cells, primary hepatocytes, and human liver needle biopsies. HBV core protein mediated the interaction with nuclear cccDNA, resulting in cytidine deamination, apurinic/apyrimidinic site formation, and finally cccDNA degradation that prevented HBV reactivation. Genomic DNA was not affected. Thus, inducing nuclear deaminases-for example, by lymphotoxin-β receptor activation-allows the development of new therapeutics that, in combination with existing antivirals, may cure hepatitis B.
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.