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Hepatitis

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...

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Related Experiment Video

Updated: Jun 24, 2026

Generation of a Humanized Mouse Liver Using Human Hepatic Stem Cells

Generation of a Humanized Mouse Liver Using Human Hepatic Stem Cells

Published on: August 29, 2016

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

Bai-Hua Zhang¹, Yuanping Zhou², Stephen Horrigan³

¹Virology, HBVtech, Rockville, Maryland, USA.

Journal of Virology

|November 6, 2025

Summary

Hepatitis B virus (HBV) infection persistence relies on covalently closed circular DNA (cccDNA). This study suggests HBV-infected cells may spontaneously clear cccDNA, halting viral replication and preventing cytopathic effects without direct targeting.

Keywords:

HBV replication cccDNA clearance and replenishment cytopathic effects persistent HBV infection

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Last Updated: Jun 24, 2026

Generation of a Humanized Mouse Liver Using Human Hepatic Stem Cells

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Published on: August 29, 2016

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

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

Published on: September 25, 2019

Area of Science:

Hepatology
Virology
Molecular Biology

Background:

Hepatitis B virus (HBV) infection establishes covalently closed circular DNA (cccDNA), which can be transient or persistent.
Persistent HBV infection requires a noncytopathic viral phenotype, often achieved by limiting viral replication within infected cells.

Purpose of the Study:

To investigate how HBV-infected cells avoid cytopathic consequences despite robust replication.
To identify the mechanism by which HBV replication is inhibited during the persistence phase.

Main Methods:

Utilized chimeric mice with humanized livers to assess HBV replication kinetics.
Quantitatively analyzed cccDNA levels in bulk cells, single nuclei, and individual HBsAg-positive cells.
Examined HBV transcription and viral protein levels.

Main Results:

HBV replication and viral product accumulation plateaued during the persistence phase.
No significant suppression of viral transcription or protein synthesis was observed.
A portion of infected cells showed undetectable cccDNA levels, suggesting spontaneous clearance.

Conclusions:

Spontaneous clearance of cccDNA may occur in HBV-infected cells, halting viral replication at its source.
This clearance mechanism could prevent uncontrolled viral replication and associated cytopathic effects.
Effective cccDNA elimination might be achievable without direct targeting of existing cccDNA, offering new therapeutic possibilities for chronic HBV infection.