ArticlePLoS pathogens2010
Generation of covalently closed circular DNA of hepatitis B viruses via intracellular recycling is regulated in a virus specific manner.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 143 citations in OpenAlex.
- Cell-based platforms for antiviral screening against hepatitis B virus: advantages, limitations, and future perspectives.Antiviral research · 2026Review
- Hepatitis B virus covalently closed circular DNA formation in murine hepatic cells uncovers a late entry block.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dynamics and Sensitivity of the Lifecycle of Hepatitis B Virus.Pathogens (Basel, Switzerland) · 2026Article
- DNA synthesis inside the hepatitis B virus creates a high-energy spool.bioRxiv : the preprint server for biology · 2026Article
- Hepatitis B Virus Nucleocapsid Assembly.Journal of molecular biology · 2025Review
- Article
- Hepatocyte-intrinsic innate immunity in hepatitis B virus infection: A focused review.World journal of hepatology · 2025Review
- Modeling of hepatitis B virus kinetics and accumulation of cccDNA in primary human hepatocytes.JHEP reports : innovation in hepatology · 2025Article
- Host 3' flap endonuclease Mus81 plays a critical role in trimming the terminal redundancy of hepatitis B virus relaxed circular DNA during covalently closed circular DNA formation.PLoS pathogens · 2025Article
- Arsenic trioxide impacts hepatitis B virus core nuclear localization and efficiently interferes with HBV infection.Microbiology spectrum · 2024Article
- Class A capsid assembly modulator apoptotic elimination of hepatocytes with high HBV core antigen levelJournal of virology · 2024Article
- Serine-arginine protein kinases and their targets in viral infection and their inhibition.Cellular and molecular life sciences : CMLS · 2023Review
- Article
- An RNA-based system to study hepatitis B virus replication and evaluate antivirals.Science advances · 2023Article
- Dynamics of Hepatitis B Virus Covalently Closed Circular DNA: A Mini-Review.Microorganisms · 2023Review
- Article
- Review
- Host cell-dependent late entry step as determinant of hepatitis B virus infection.PLoS pathogens · 2022Article
- Region-Specific Hepatitis B Virus Genome Exposure from Nucleocapsid Modulated by Capsid Linker Sequence and Inhibitor: Implications for Uncoating.Journal of virology · 2022Article
- Structure-Based Discovery ofViruses · 2022Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistence of hepatitis B virus (HBV) infection requires covalently closed circular (ccc)DNA formation and amplification, which can occur via intracellular recycling of the viral polymerase-linked relaxed circular (rc) DNA genomes present in virions. Here we reveal a fundamental difference between HBV and the related duck hepatitis B virus (DHBV) in the recycling mechanism. Direct comparison of HBV and DHBV cccDNA amplification in cross-species transfection experiments showed that, in the same human cell background, DHBV but not HBV rcDNA converts efficiently into cccDNA. By characterizing the distinct forms of HBV and DHBV rcDNA accumulating in the cells we find that nuclear import, complete versus partial release from the capsid and complete versus partial removal of the covalently bound polymerase contribute to limiting HBV cccDNA formation; particularly, we identify genome region-selectively opened nuclear capsids as a putative novel HBV uncoating intermediate. However, the presence in the nucleus of around 40% of completely uncoated rcDNA that lacks most if not all of the covalently bound protein strongly suggests a major block further downstream that operates in the HBV but not DHBV recycling pathway. In summary, our results uncover an unexpected contribution of the virus to cccDNA formation that might help to better understand the persistence of HBV infection. Moreover, efficient DHBV cccDNA formation in human hepatoma cells should greatly facilitate experimental identification, and possibly inhibition, of the human cell factors involved in the process.
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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.