ArticleJHEP reports : innovation in hepatology2025
Modeling of hepatitis B virus kinetics and accumulation of cccDNA in primary human hepatocytes.
Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed.
- HBV serum RNA kinetics during nucleic acid polymers based therapy predict functional cure.Antiviral research · 2025Trial
- Cell-based platforms for antiviral screening against hepatitis B virus: advantages, limitations, and future perspectives.Antiviral research · 2026Review
- Early hepatitis B and delta virus kinetics in patients undergoing liver transplantation.Scientific reports · 2026Article
- Clinical trial simulation of antiviral drugs.Journal of virology · 2026Review
- Dynamics and Sensitivity of the Lifecycle of Hepatitis B Virus.Pathogens (Basel, Switzerland) · 2026Article
- Serum PreS1 antigen combined with vascular endothelial growth factor can identify low-level hepatitis B virus DNA replication in patients with hepatitis B e antigen-negative chronic infection.American journal of translational research · 2026Article
- Modeling of hepatitis B virus infection spread in primary human hepatocytes.Journal of virology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Background & Aims: Knowledge about early HBV covalently closed circular DNA (cccDNA) accumulation post infection is lacking. We characterized and mathematically modeled HBV infection kinetics during early infection and treatment in primary human hepatocytes (PHHs). Methods: PHHs were inoculated with HBV, and infection was monitored with and without treatment with the nucleoside analog entecavir (ETV), the HBV-entry inhibitor Myr-preS1, or both ETV + Myr-preS1. Extracellular HBV DNA (exHBV), total intracellular HBV DNA (inHBV), and cccDNA were frequently measured during the 12 days post inoculation. A multicompartmental mathematical model was developed to explain HBV infection dynamics. Results: Multiphasic exHBV and inHBV kinetics were overall similar in untreated and Myr-preS1-treated PHHs. In ETV-treated PHHs (either alone or with Myr-preS1), exHBV and inHBV initially declined and did not resurge. ETV-treated cultures had significantly ( Conclusions: The study provides insight into the interrelationships and dynamics of cccDNA accumulation, inHBV accumulation, and secretion of exHBV containing particles. Although kinetics and modeling support the conclusion that the level of cccDNA in the cell is regulated, the mechanisms that determine HBV capsid secretion Impact and implications: Using primary human hepatocytes (PHHs), we characterize early HBV kinetics post infection. HBV-infected PHH were treated with an entry inhibitor to characterize the accumulation of intracellular and extracellular HBV DNA and the nuclear episomal viral genome called covalently closed circular DNA (cccDNA) in the absence of HBV spread. Kinetic and mathematical modeling in PHHs confirms that the replication inhibitor, entecavir, strongly blocks intracellular HBV DNA accumulation, which also slowed the accumulation of cccDNA. However, modeling indicates that effects on cccDNA accumulation are not directly determined by intracellular HBV DNA levels, supporting the conclusion that cccDNA levels within the cell are regulated in some yet-to-be-elucidated manner.
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