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A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
Published on: May 10, 2022
Short-chain Fatty Acids and Bile Acids Signaling in Chronic Hepatitis B
Siqi Sun1, Sisi Yang1, Yihe Yu1
1State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Department of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Journal of Clinical and Translational Hepatology
|July 22, 2026
Summary
Gut microbiota metabolites like short-chain fatty acids and bile acids show promise for a functional cure in chronic hepatitis B. Targeting these molecules may overcome immune tolerance and improve treatment outcomes for this global health challenge.
Area of Science:
- Hepatology and immunology
- Microbiome research
- Virology
Background:
- Chronic hepatitis B (CHB) is a significant global health issue with limited functional cure rates using current therapies.
- Existing treatments primarily focus on viral suppression, with few patients achieving sustained hepatitis B surface antigen loss.
- The gut-liver axis and its metabolites are emerging as key players in HBV infection and immune regulation.
Purpose of the Study:
- To review the biological characteristics and mechanistic roles of short-chain fatty acids (SCFAs) and bile acids (BAs) in CHB.
- To explore the translational relevance of SCFAs and BAs as therapeutic targets for overcoming immune tolerance in CHB.
- To propose strategies for improving functional cure rates in CHB.
Main Methods:
- Review of in vitro and animal studies on SCFAs and BAs in HBV infection.
- Analysis of the mechanistic roles of SCFAs (e.g., butyrate) in suppressing HBV gene expression and modulating host immunity.
- Examination of the signaling hub involving farnesoid X receptor, Takeda G protein-coupled receptor 5, and sodium taurocholate cotransporting polypeptide in BA-mediated effects.
Main Results:
- SCFAs, such as butyrate, can suppress HBV gene expression by inhibiting histone deacetylases and remodeling HBV DNA minichromatin.
- SCFAs may enhance antiviral immunity but can also reinforce immune tolerance in specific contexts.
- Bile acids interact with key receptors, influencing HBV replication and host responses, with early studies showing potential for hepatitis B surface antigen reduction with FXR agonists.
Conclusions:
- Gut microbiota metabolites (SCFAs and BAs) represent promising therapeutic targets for achieving a functional cure in CHB.
- Targeting the gut-liver axis offers a novel approach to overcome immune tolerance in CHB.
- Biomarker-guided stratification and multi-target combination therapies are proposed to enhance functional cure rates for CHB patients.
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