ArticleProceedings of the National Academy of Sciences of the United States of America2003
Transcriptional and posttranscriptional control of hepatitis B virus gene expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 73 citations in OpenAlex.
- Serum hepatitis B virus RNA predicts response to peginterferon treatment in HBeAg-positive chronic hepatitis B.Journal of viral hepatitis · 2020Trial
- Altered expression of ADAR1, N4BP1, and PSME1 in PBMCs correlated with therapeutic outcomes in HBeAg-negative chronic hepatitis B patients treated with Peg-IFN-α.Frontiers in cellular and infection microbiology · 2026Observational
- Dynamic changes in IFI44L and SAMHD1 mRNA levels in PBMCs are associated with treatment response in HBeAg-negative chronic hepatitis B during peg-IFN-α therapy.Frontiers in microbiology · 2026Article
- Altered expression of MX2 and SAMD4A in PBMCs predicts early treatment responses in HBeAg-positive chronic hepatitis B patients during Peg-IFN-α therapy.Frontiers in pharmacology · 2026Article
- Interferon alpha-inducible protein 27 (IFI27) inhibits hepatitis B virus (HBV) transcription through downregulating cellular transcription factor C/EBPα.Journal of virology · 2025Article
- HBV cccDNA: The Molecular Reservoir of Hepatitis B Persistence and Challenges to Achieve Viral Eradication.Biomolecules · 2025Review
- Review
- β-Catenin Signaling Regulates theJournal of virology · 2021Article
- Innate immunity and HBV persistence.Current opinion in virology · 2021Review
- Interferon-induced degradation of the persistent hepatitis B virus cccDNA form depends on ISG20.EMBO reports · 2021Article
- cccDNA Maintenance in Chronic Hepatitis B - Targeting the Matrix of Viral Replication.Infection and drug resistance · 2020Review
- Revisiting Hepatitis B Virus: Challenges of Curative Therapies.Journal of virology · 2019Review
- Cell and Animal Models for Studying Hepatitis B Virus Infection and Drug Development.Gastroenterology · 2019Review
- Type I Interferon Signaling Prevents Hepatitis B Virus-Specific T Cell Responses by Reducing Antigen Expression.Journal of virology · 2018Article
- Flavocoxid exerts a potent antiviral effect against hepatitis B virus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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
- The Role of cccDNA in HBV Maintenance.Viruses · 2017Review
- T cell--associated immunoregulation and antiviral effect of oxymatrine in hydrodynamic injection HBV mouse model.Acta pharmaceutica Sinica. B · 2017Article
- Interferon-inducible ribonuclease ISG20 inhibits hepatitis B virus replication through directly binding to the epsilon stem-loop structure of viral RNA.PLoS pathogens · 2017Article
- Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation.PLoS pathogens · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hepatitis B virus (HBV) infects humans and certain nonhuman primates. Viral clearance and acute disease are associated with a strong, polyclonal, multispecific cytotoxic T lymphocyte response. Infiltrating T cells, as well as other activated inflammatory cells, produce cytokines that can regulate hepatocellular gene expression. Using an HBV transgenic mouse model, our laboratory has previously demonstrated that adoptive transfer of HBV-specific cytotoxic T lymphocytes or injection of IL-2 can noncytopathically inhibit HBV gene expression by a posttranscriptional IFN-gamma- and/or tumor necrosis factor alpha-dependent mechanism. Here, we report that HBV gene expression can also be controlled at the posttranscriptional level during persistent lymphocytic choriomeningitis virus infection. In contrast, it is controlled at the transcriptional level during acute murine cytomegalovirus infection or after repetitive polyinosinic-polycytidylic acid injection. Finally, we show that transcriptional inhibition of HBV is associated with changes in liver-specific gene expression. These results elucidate pathways that regulate the viral life cycle and suggest additional approaches for the treatment of chronic HBV infection.
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.