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Updated: Jun 6, 2026

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
Adiponectin, a downstream target gene of peroxisome proliferator-activated receptor γ, controls hepatitis B virus
Sarah Yoon1, Jaesung Jung, Taeyeung Kim
1Department of Microbiology, Ajou University School of Medicine, Woncheon-dong 5, Suwon 442-721, South Korea.
Abstract:
In this study, HepG2-hepatitis B virus (HBV)-stable cells that did not overexpress HBx and HBx-deficient mutant-transfected cells were analyzed for their expression of HBV-induced, upregulated adipogenic and lipogenic genes. The mRNAs of CCAAT enhancer binding protein α (C/EBPα), peroxisome proliferator-activated receptor γ (PPARγ), adiponectin, liver X receptor α (LXRα), sterol regulatory element binding protein 1c (SREBP1c), and fatty acid synthase (FAS) were expressed at higher levels in HepG2-HBV and lamivudine-treated stable cells and HBx-deficient mutant-transfected cells than in the HepG2 cells. Lamivudine treatment reduced the mRNA levels of PPARγ and C/EBPα. Conversely, HBV replication was upregulated by adiponectin and PPARγ agonist rosiglitazone treatments and was downregulated by adiponectin siRNAs. Collectively, our results demonstrate that HBV replication and/or protein expression, even in the absence of HBx, upregulated adipogenic or lipogenic genes, and that the control of adiponectin might prove useful as a therapeutic modality for the treatment of chronic hepatitis B.
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