ArticleJournal of virology2011
Roles of the envelope proteins in the amplification of covalently closed circular DNA and completion of synthesis of the plus-strand DNA in hepatitis B virus.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 78 citations in OpenAlex.
- Peripheral Biomarkers in Chronic Hepatitis D Infection: A Review.Journal of viral hepatitis · 2026Review
- Dynamics and Sensitivity of the Lifecycle of Hepatitis B Virus.Pathogens (Basel, Switzerland) · 2026Article
- HBVZ10, an AAV8 vector-based new HBV therapy candidate for cccDNA elimination.Molecular therapy. Methods & clinical development · 2025Article
- Replication-driven HBV cccDNA loss in chimeric mice with humanized livers.Journal of virology · 2025Article
- The HBV variant CpF97L supports the secretion of pgRNA-containing virions at a level much greater than WT HBV.Journal of virology · 2025Article
- Hepatitis B Surface Antigen Isoforms: Their Clinical Implications, Utilisation in Diagnosis, Prevention and New Antiviral Strategies.Pathogens (Basel, Switzerland) · 2024Review
- Article
- Pathogenicity and virulence of Hepatitis B virus.Virulence · 2022Review
- Drug Discovery Study Aimed at a Functional Cure for HBV.Viruses · 2022Review
- Regulation of Hepatitis B Virus Virion Release and Envelopment Timing by Nucleocapsid and Envelope Interactions.Journal of virology · 2022Article
- Mechanism of Hepatitis B Virus cccDNA Formation.Viruses · 2021Review
- Toward a new era of hepatitis B virus therapeutics: The pursuit of a functional cure.World journal of gastroenterology · 2021Review
- Regulation of Hepatitis B Virus Replication by Cyclin Docking Motifs in Core Protein.Journal of virology · 2021Article
- Multiple roles of PP2A binding motif in hepatitis B virus core linker and PP2A in regulating core phosphorylation state and viral replication.PLoS pathogens · 2021Article
- Animal Models for the Study of Hepatitis B Virus Pathobiology and Immunity: Past, Present, and Future.Frontiers in microbiology · 2021Review
- Identification of infectious spleen and kidney necrosis virus (ISKNV)-encoded microRNAs.Virus genes · 2020Article
- New Insights on Molecular Mechanism of Hepatitis B Virus Covalently Closed Circular DNA Formation.Cells · 2020Review
- Hepatitis B virus cccDNA: Formation, regulation and therapeutic potential.Antiviral research · 2020Review
- Role of Hepatitis B virus capsid phosphorylation in nucleocapsid disassembly and covalently closed circular DNA formation.PLoS pathogens · 2020Article
- Revisiting Hepatitis B Virus: Challenges of Curative Therapies.Journal of virology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Covalently closed circular DNA (cccDNA), the nuclear form of hepatitis B virus (HBV), is synthesized by repair of the relaxed circular (RC) DNA genome. Initially, cccDNA is derived from RC DNA from the infecting virion, but additional copies of cccDNA are derived from newly synthesized RC DNA molecules in a process termed intracellular amplification. It has been shown that the large viral envelope protein limits the intracellular amplification of cccDNA for duck hepatitis B virus. The role of the envelope proteins in regulating the amplification of cccDNA in HBV is not well characterized. The present report demonstrates regulation of synthesis of cccDNA by the envelope proteins of HBV. Ablation of expression of the envelope proteins led to an increase (>6-fold) in the level of cccDNA. Subsequent restoration of envelope protein expression led to a decrease (>50%) in the level of cccDNA, which inversely correlated with the level of the envelope proteins. We found that the expression of L protein alone or in combination with M and/or S proteins led to a decrease in cccDNA levels, indicating that L contributes to the regulation of cccDNA. Coexpression of L and M led to greater regulation than either L alone or L and S. Coexpression of all three envelope proteins was also found to limit completion of plus-strand DNA synthesis, and the degree of this effect correlated with the level of the proteins and virion secretion.
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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.