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A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
Published on: May 10, 2022
Curcumin inhibits hepatitis B virus via down-regulation of the metabolic coactivator PGC-1alpha
Maya Mouler Rechtman1, Ofir Har-Noy, Iddo Bar-Yishay
1The Institute of Gastroenterology and Liver Disease, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
Abstract:
Hepatitis B virus (HBV) infects the liver and uses its cell host for gene expression and propagation. Therefore, targeting host factors essential for HBV gene expression is a potential anti-viral strategy. Here we show that treating HBV expressing cells with the natural phenolic compound curcumin inhibits HBV gene expression and replication. This inhibition is mediated via down-regulation of PGC-1alpha, a starvation-induced protein that initiates the gluconeogenesis cascade and that has been shown to robustly coactivate HBV transcription. We suggest curcumin as a host targeted therapy for HBV infection that may complement current virus-specific therapies.
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