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Updated: May 7, 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

A mouse model for HBV immunotolerance and immunotherapy.

Dan Yang¹, Longchao Liu¹, Danming Zhu²

¹1] IBP-UC Group for Immunotherapy, CAS Key Laboratory for Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China [2] University of Chinese Academy of Sciences, Beijing 100049, China.

Cellular & Molecular Immunology

|October 1, 2013

Summary

A new mouse model with sustained hepatitis B virus (HBV) viremia was developed. This model, treated with HBsAg/CpG, showed clearance of HBV and induced immune responses, offering a tool for studying HBV immunotolerance and developing therapies.

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

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Published on: January 7, 2019

Area of Science:

Immunology
Virology
Hepatology

Background:

Studying hepatitis B virus (HBV) immunotolerance and immunopathogenesis is hindered by the lack of suitable small animal models.
Clinical HBV carriers often exhibit immune tolerance, making them resistant to conventional vaccines.

Purpose of the Study:

To develop a small animal model that recapitulates HBV infection and associated immune tolerance.
To evaluate a novel vaccine strategy for overcoming HBV-induced immune tolerance.

Main Methods:

A recombinant adeno-associated virus (AAV) carrying a replicable HBV genome (AAV/HBV) was used to establish a mouse model with sustained HBV viremia.
Mice were immunized with HBV surface antigen (HBsAg) combined with the TLR9 agonist CpG as an adjuvant.
Immune responses, HBV markers (viremia, liver replication, protein expression), and antibody production were assessed.

Main Results:

The AAV/HBV mouse model exhibited sustained viremia and immune tolerance, similar to human HBV carriers.
Conventional HBV vaccination failed to induce an immune response in AAV/HBV-infected mice.
HBsAg/CpG vaccination successfully induced HBV-specific antibody production, T-cell responses, and clearance of HBV viremia.
HBV DNA replication and protein expression in the liver were significantly reduced post-vaccination.

Conclusions:

The AAV/HBV mouse model provides a robust platform for studying HBV immunotolerance mechanisms.
The HBsAg/CpG vaccine strategy demonstrates potential for overcoming HBV-induced immune tolerance and eradicating HBV infection.
This model can aid in the development of novel immunotherapies for chronic HBV infections.