Related Experiment Video
Updated: May 8, 2026
07:25
Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
Published on: September 25, 2019
Understanding HBV immunopathogenesis to inform future immune-based therapies
Margaux Bossis1, Phuong-Ha Le2, Tarik Asselah3
1Institut de Recherche Saint-Louis, Université Paris Cité, Inserm U1342, Paris, France.
Antiviral Research
|May 7, 2026
Summary
Chronic hepatitis B (HBV) infection persists despite vaccines, causing liver disease. New therapies aim to restore HBV-specific immune responses for a functional cure, not just viral suppression.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- Chronic hepatitis B virus (HBV) infection affects over 250 million globally, leading to cirrhosis and hepatocellular carcinoma (HCC).
- Current treatments suppress HBV replication but rarely achieve functional cure (sustained HBsAg loss post-treatment).
- Viral persistence is driven by intrahepatic HBV DNA and immune dysfunction.
Purpose of the Study:
- To review HBV immunopathogenesis in acute and chronic infections.
- To explore immune correlates of functional cure.
- To discuss immune-based therapies and combination strategies for HBV.
Main Methods:
- Review of current understanding of HBV immunopathogenesis.
- Analysis of immune dysfunction in chronic HBV.
- Discussion of clinical trials for immune-based therapies.
Main Results:
- HBV infection involves a tolerogenic liver microenvironment and impaired immune responses.
- Immune dysfunction includes impaired innate sensing and progressive dysfunction of HBV-specific B and T cells.
- Functional cure is associated with restored polyfunctional T cells and liver immune remodeling.
Conclusions:
- Achieving functional cure for chronic HBV requires addressing viral replication, antigen load, and immune responses.
- Combination strategies coupling antigen reduction with immune restoration are emerging.
- Durable off-treatment control necessitates a multifaceted approach targeting both the virus and the host immune system.
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