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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.

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Related Experiment Video

Updated: May 6, 2026

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

Published on: February 3, 2012

Chronic Hepatitis B Genotype C Mouse Model with Persistent Covalently Closed Circular DNA.

Deok-Hwa Seo¹, Wonhee Hur², Juhee Won³

¹The Catholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.

|January 8, 2025

Summary

A new mouse model effectively replicates chronic Hepatitis B virus (HBV) infection, enabling study of HBV cccDNA persistence. This breakthrough aids research into therapies targeting the viral DNA reservoir.

Keywords:

Hepatitis B virus cccDNA chronic HBV infection genotype C mouse model

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Last Updated: May 6, 2026

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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:

Chronic Hepatitis B virus (HBV) infection poses significant mortality risks due to cirrhosis and hepatocellular carcinoma (HCC).
Covalently closed circular DNA (cccDNA) is a persistent viral DNA reservoir in hepatocytes, driving continuous HBV replication and treatment resistance.
Existing animal models inadequately replicate cccDNA dynamics, hindering research into HBV pathogenesis and therapeutics.

Purpose of the Study:

To develop and validate a novel mouse model for investigating Hepatitis B virus cccDNA formation and maintenance.
To establish a platform for evaluating therapeutic strategies targeting the HBV cccDNA reservoir.

Main Methods:

Infection of C57BL/6 mice with recombinant adeno-associated virus (rAAV) carrying a 1.3-overlength HBV genome (genotype C).
Assessment of cccDNA levels and viral replication markers (HBsAg, HBeAg, HBV DNA) at various time points.
Quantitative PCR (qPCR) with selective DNase treatment and Southern blot analysis for cccDNA detection.

Main Results:

Successful establishment of a chronic HBV mouse model with persistent cccDNA expression in hepatocytes.
Sustained elevation of serum HBsAg and HBeAg for up to 12 weeks with normal alanine transaminase (ALT) levels.
Confirmation of HBV DNA expression and detection of cccDNA using qPCR and Southern blot analysis.

Conclusions:

The rAAV-HBV1.3 mouse model effectively recapitulates key aspects of chronic HBV infection, including cccDNA persistence.
This model serves as a valuable tool for studying long-term cccDNA maintenance and for preclinical testing of novel anti-HBV therapies targeting cccDNA.