Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

HBVZ10, an AAV8 vector-based new HBV therapy candidate for cccDNA elimination.

Molecular therapy. Methods & clinical development·2025
Same author

Replication-driven HBV cccDNA loss in chimeric mice with humanized livers.

Journal of virology·2025
Same author

HBsAg decline and clearance with peg-IFN therapy added to nucleos(t)ide analogues: an individual participant data meta-analysis of prospective trials (PROSPER).

Gut·2025
Same author

Best practices for screening, testing, diagnosing, and treating patients with hepatitis D (delta) virus based on global expert review and recent guidelines.

Antiviral therapy·2025
Same author

IFN-β production promotes metabolic rewiring and protection against oxidative stress in hepatitis delta virus-infected hepatocyte cultures.

Cell death & disease·2025
Same author

Mortality risk in migrant and non-migrant individuals with chronic hepatitis B virus infection: a French hospital-based cohort study (ANRS CO22 HEPATHER).

BMC global and public health·2025

Related Experiment Video

Updated: Jul 5, 2025

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
07:25

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice

Published on: September 25, 2019

6.9K

Replication-driven HBV cccDNA loss in chimeric mice with humanized livers.

Bai-Hua Zhang, Yuanping Zhou, Ben Tempel

    Biorxiv : the Preprint Server for Biology
    |January 18, 2024
    PubMed
    Summary

    Hepatitis B virus (HBV) infection involves stable viral DNA (cccDNA). Blocking its replenishment causes significant cccDNA loss, offering a new elimination strategy.

    More Related Videos

    A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
    10:56

    A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes

    Published on: September 15, 2018

    8.2K
    Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis
    00:10

    Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis

    Published on: September 11, 2019

    8.6K

    Related Experiment Videos

    Last Updated: Jul 5, 2025

    Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
    07:25

    Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice

    Published on: September 25, 2019

    6.9K
    A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
    10:56

    A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes

    Published on: September 15, 2018

    8.2K
    Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis
    00:10

    Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis

    Published on: September 11, 2019

    8.6K

    Area of Science:

    • Hepatology
    • Virology
    • Molecular Biology

    Background:

    • Hepatitis B virus (HBV) infection establishes stable, nuclear covalently closed circular DNA (cccDNA).
    • Eliminating HBV requires targeting cccDNA or infected cells, which is challenging.
    • HBV-infected cells can undergo cytopathic destruction, leading to cccDNA loss.

    Purpose of the Study:

    • To investigate cccDNA dynamics in HBV-infected humanized liver chimeric mice.
    • To explore the relationship between viral replication, cell fate, and cccDNA stability.
    • To evaluate a novel strategy for HBV elimination by blocking cccDNA replenishment.

    Main Methods:

    • Utilized HBV-infected chimeric mice with humanized livers.
    • Monitored cccDNA levels during viral replication and infection phases.
    • Intervened by blocking cccDNA replenishment pathways.

    Main Results:

    • HBV-infected cells exhibit replication, viral product retention, and eventual cytopathic destruction with cccDNA loss.
    • Replication-driven cccDNA loss occurs during both infection spread and persistence.
    • Blocking cccDNA replenishment pathways reduced cccDNA levels by over 100-fold.

    Conclusions:

    • HBV-infected cells struggle to maintain cccDNA while remaining noncytopathic.
    • Spontaneous cccDNA loss can be leveraged for elimination by blocking replenishment.
    • This approach offers an unconventional strategy for progressive cccDNA elimination without directly targeting cccDNA.