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Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
Published on: September 25, 2019
Hepatitis B virus core antigen determines viral persistence in a C57BL/6 mouse model
Yi-Jiun Lin1, Li-Rung Huang, Hung-Chih Yang
1Graduate Institute of Microbiology, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei 10002, Taiwan.
Summary
Hepatitis B virus (HBV) persistence in mice depends on the core antigen (HBcAg). A specific 10-amino acid region of HBcAg is crucial for viral clearance and immune response, impacting HBV persistence.
Area of Science:
- Virology
- Immunology
- Hepatology
Background:
- Hepatitis B virus (HBV) infection can lead to chronic liver disease.
- Understanding the mechanisms of HBV persistence is crucial for developing effective treatments.
- A mouse model of HBV persistence was previously established.
Purpose of the Study:
- To identify viral antigens critical for maintaining HBV persistence.
- To investigate the role of the hepatitis B core antigen (HBcAg) in HBV persistence.
- To map the specific region of HBcAg involved in viral clearance.
Main Methods:
- Development of a mouse model using hydrodynamic injection of HBV DNA.
- Generation of HBV mutants with gene knockouts in core, HBeAg, HBx, and polymerase.
- Construction of serial HBcAg deletion mutants to identify critical regions.
- Monitoring of HBV replication, antigenemia, and immune responses (IFN-gamma).
Main Results:
- Mice receiving HBcAg-mutated HBV showed high levels of hepatitis B surface antigenemia and prolonged HBsAg expression.
- A specific 10-amino acid region at the carboxyl terminus of HBcAg (aa 176-185) was identified as essential for viral clearance.
- Mice with mutations in this HBcAg region failed to elicit a proper HBcAg-specific IFN-gamma response and maintained HBV virions for 6 months.
Conclusions:
- The hepatitis B core antigen (HBcAg) plays a critical role in determining HBV persistence.
- The immune response to HBcAg, particularly the IFN-gamma response, is essential for controlling HBV replication.
- The carboxyl-terminal region of HBcAg (aa 176-185) is vital for eliciting an effective anti-HBV immune response and achieving viral clearance.
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