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Published on: June 26, 2019
Identification of Cyclin L1 as a Host Factor Regulating Hepatitis B Virus Replication
Collins Oduor Owino1,2,3, Balakrishnan Chakrapani Narmada1,4, Gian Yi Lin4
1Laboratory of Precision Medicine and Cancer Evolution, Genome Institute of Singapore, Agency for Science, Technology, and Research (A*STAR), 60 Biopolis St., #02-01 Genome, Singapore 138672, Singapore.
Viruses
|May 27, 2026
Summary
Cyclin L1 (CCNL1) promotes hepatitis B virus (HBV) replication by regulating RNA polymerase II activity and chromatin accessibility at the HBV cccDNA. Targeting CCNL1 may offer a novel therapeutic strategy for chronic HBV infection.
Area of Science:
- Hepatology
- Virology
- Molecular Biology
Background:
- Hepatitis B virus (HBV) infection is a significant global health concern, necessitating novel therapeutic strategies for a functional cure.
- Understanding host-viral interactions is crucial for developing targeted antiviral therapies against HBV.
- HBV relies on host cellular machinery for its replication and persistence.
Purpose of the Study:
- To identify host factors that regulate HBV transcription and replication.
- To elucidate the mechanism by which host factors influence HBV gene expression.
- To evaluate cyclin L1 (CCNL1) as a potential therapeutic target for HBV.
Main Methods:
- Whole-transcriptome sequencing (WTS) of HBV-infected primary human hepatocytes (PHH).
- RNA interference (RNAi)-based functional screening of dysregulated host genes.
- Analysis of RNA polymerase II (RNAPII) phosphorylation and chromatin modifications at HBV cccDNA.
- Expression analysis of CCNL1 in chronic hepatitis B patients.
Main Results:
- CCNL1 was identified as a key host factor promoting HBV replication.
- CCNL1 knockdown reduced HBV gene expression, including HBsAg.
- CCNL1 regulates RNAPII phosphorylation (Ser2) and chromatin accessibility (H3ac, H3K27ac) at HBV cccDNA.
- Elevated CCNL1 expression was observed in chronic hepatitis B patients.
Conclusions:
- CCNL1 promotes HBV transcription and replication by modulating RNAPII activity and chromatin structure.
- CCNL1 is a host susceptibility factor for HBV infection.
- Targeting CCNL1 represents a potential therapeutic strategy for chronic HBV.
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