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TGF-β triggers HBV cccDNA degradation through AID-dependent deamination
Ying Qiao1, Xiaoxu Han2, Gefei Guan3
1The Core Laboratory for Public Health Science and Practice, The First Affiliated Hospital, China Medical University, Shenyang, China.
FEBS Letters
|February 13, 2016
Summary
Hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) is degraded by transforming growth factor-beta (TGF-β) through activation-induced cytidine deaminase (AID) and uracil-DNA glycosylase (UNG) in liver cells, offering a new strategy for cccDNA elimination.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- The covalently closed circular DNA (cccDNA) of hepatitis B virus (HBV) is central to viral persistence.
- Cellular factors restricting HBV cccDNA remain largely unidentified.
Purpose of the Study:
- To elucidate the cellular mechanisms involved in the restriction of nuclear HBV cccDNA.
- To investigate the role of transforming growth factor-beta (TGF-β) in controlling HBV cccDNA.
Main Methods:
- Hepatocyte culture models were used to study HBV cccDNA.
- The roles of activation-induced cytidine deaminase (AID) and uracil-DNA glycosylase (UNG) in cccDNA degradation were assessed.
- The influence of HBV core protein on AID-cccDNA interaction was examined.
Main Results:
- Transforming growth factor-beta (TGF-β) induces nuclear HBV cccDNA degradation and hypermutation in hepatocytes.
- This process relies on the deamination activity of AID and the excision activity of uracil-DNA glycosylase (UNG).
- HBV core protein facilitates the interaction between AID and viral cccDNA, enhancing degradation.
Conclusions:
- A novel innate immune mechanism involving TGF-β restricts nuclear HBV cccDNA.
- The concerted action of AID and UNG, promoted by HBV core protein, degrades viral cccDNA.
- This pathway suggests a potential therapeutic strategy for HBV cccDNA elimination.
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