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Related Experiment Video

Updated: Jul 19, 2026

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells

Published on: June 5, 2020

PGC-1alpha controls hepatitis B virus through nutritional signals.

Amir Shlomai¹, Nir Paran, Yosef Shaul

¹Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot 76100, Israel.

Proceedings of the National Academy of Sciences of the United States of America

|October 18, 2006

Summary

Hepatitis B virus (HBV) gene expression is controlled by the body's nutritional status. The metabolic regulator PGC-1alpha (peroxisome proliferator-activated receptor-gamma coactivator 1alpha) links nutrition signaling to HBV replication.

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Area of Science:

Virology
Hepatology
Metabolic Regulation

Background:

Hepatitis B virus (HBV) replicates in the liver, relying on liver-enriched nuclear receptors (NRs) for viral gene expression.
NRs are crucial for metabolic processes like gluconeogenesis and fatty acid oxidation, but their link to HBV gene expression is unclear.

Purpose of the Study:

To investigate the association between metabolic regulation and HBV gene expression.
To determine the role of PGC-1alpha and hepatocyte nuclear factor 4alpha in HBV transcription.

Main Methods:

Investigated the coactivation of HBV transcription by PGC-1alpha.
Examined the role of hepatocyte nuclear factor 4alpha in HBV transcription.
Studied the in vivo effect of fasting and refeeding on HBV gene expression in a mouse model.

Main Results:

PGC-1alpha robustly coactivates HBV transcription.
Hepatocyte nuclear factor 4alpha plays a significant role in PGC-1alpha-mediated HBV transcription.
Short-term fasting induces HBV gene expression in vivo, which is reversible by refeeding and dependent on PGC-1alpha.

Conclusions:

HBV gene expression is tightly regulated by nutritional state via the metabolic regulator PGC-1alpha.
Metabolism plays a critical role in virus-host interactions by influencing viral gene expression and life cycle.