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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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Updated: Jun 13, 2026

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

Application of hepatitis B virus replication mouse model.

Zhan Gao¹, Feng-Jun Liu, Li Liu

¹Center of Infectious Diseases, West China Hospital of Sichuan University, Chengdu, Sichuan Province, China.

World Journal of Gastroenterology

|April 27, 2010

Summary

This study validates a hepatitis B virus (HBV) replication mouse model for assessing antiviral efficacy and studying HBV mutant replication. The model proved valuable for evaluating drug effectiveness and understanding drug-resistant HBV mutants in vivo.

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Last Updated: Jun 13, 2026

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Published on: February 1, 2017

Area of Science:

Hepatology
Virology
Infectious Diseases

Background:

Hepatitis B virus (HBV) infection poses a significant global health burden.
Studying HBV replication and developing effective antiviral therapies remain critical challenges.
Existing models for HBV research have limitations in fully recapitulating viral biology and treatment responses.

Purpose of the Study:

To evaluate the utility of a newly established HBV replication mouse model.
To assess the model's capability in detecting the efficacy of antiviral agents against HBV.
To determine the model's value in studying the replication of HBV drug-resistant mutants and HBx-deficient variants.

Main Methods:

Mice were infected with wild-type HBV plasmid (pHBV4.1) and treated with antiviral agents: polyinosinic-polytidylin acid (polyIC), adefovir, and entecavir.
The inhibitory effects of these agents on HBV DNA replication intermediates were quantified.
The model's performance was further assessed using HBV drug-resistant mutants (telbivudine and adefovir resistance) and an HBx-minus mutant.

Main Results:

Entecavir demonstrated significant inhibition (13.6-fold) of HBV DNA replication intermediates, while adefovir showed moderate inhibition (1.4-fold) and polyIC showed minimal reduction (1-fold).
HBV DNA replication intermediates were detectable in models with telbivudine-resistant (4.5-fold decrease), adefovir-resistant (5.6-fold decrease), and HBx-minus mutants (2.9-fold decrease) compared to wild-type HBV.
These findings indicate differential impacts of mutations and treatments on viral replication within the mouse model.

Conclusions:

The established HBV replication mouse model is a practical and effective tool for evaluating antiviral drug efficacy in vivo.
The model facilitates the study of HBV replication dynamics, including the behavior of drug-resistant mutants and HBx-deficient variants.
This model offers a valuable platform for advancing research in HBV biology and therapeutic development.