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Updated: Sep 11, 2025
09:02
Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
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Long noncoding RNA HNF4A-AS1 upregulates TLE4 to inhibit hepatitis B virus replication
Lihua Liu1, Wenxiu Dai2, Qinghui Wang2
1Department of clinical laboratory, Wuxi Second People's Hospital, the Affiliated Central Hospital of Jiangnan University, Wuxi 214000, China.
Virus Research
|August 15, 2025
Summary
Hepatitis B virus (HBV) infection downregulates HNF4A-AS1, a long noncoding RNA. HNF4A-AS1 inhibits HBV replication by boosting TLE4, acting as a host restriction factor and potential therapeutic target.
Area of Science:
- Molecular biology
- Virology
- Hepatology
Background:
- Long noncoding RNAs (lncRNAs) play roles in hepatitis B virus (HBV) replication.
- The specific functions of most lncRNAs in HBV replication are not well understood.
Purpose of the Study:
- To investigate the role of HNF4A-AS1 in HBV replication.
- To elucidate the mechanism by which HNF4A-AS1 affects HBV.
Main Methods:
- Studied the expression of HNF4A-AS1 in HBV-infected human hepatoma cells.
- Assessed the effect of HNF4A-AS1 on HBV transcription and replication.
- Investigated the interaction between HNF4A-AS1 and TLE4.
Main Results:
- HBV infection downregulated HNF4A-AS1 expression.
- HNF4A-AS1 inhibited HBV transcription and replication.
- HNF4A-AS1 promoted TLE4 expression transcriptionally.
- The WD-repeat domain of TLE4 was crucial for its anti-HBV activity.
Conclusions:
- HNF4A-AS1 acts as a host restriction factor against HBV replication.
- A negative feedback mechanism exists between HBV replication and HNF4A-AS1 expression.
- HNF4A-AS1 and TLE4 represent potential therapeutic targets for HBV treatment.
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