Curcumin inhibits hepatitis B virus via down-regulation of the metabolic coactivator PGC-1alpha.
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.
Rechtman
Maya Mouler
MM
The Institute of Gastroenterology and Liver Disease, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
Har-Noy
Ofir
O
Bar-Yishay
Iddo
I
Fishman
Sigal
S
Adamovich
Yaarit
Y
Shaul
Yosef
Y
Halpern
Zamir
Z
Shlomai
Amir
A
D000998:Antiviral Agents / Q000378:metabolism; D001669:Biochemical Phenomena; D003474:Curcumin / Q000378:metabolism*; D015536:Down-Regulation; D015870:Gene Expression; D005943:Gluconeogenesis / Q000235:genetics; D006509:Hepatitis B / Q000235:genetics / Q000378:metabolism* / Q000821:virology; D006515:Hepatitis B virus / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D008099:Liver / Q000378:metabolism* / Q000821:virology; D010434:Pepsin A
D000998:Antiviral Agents; D010434:Pepsin A; C020557:gastricsin; D003474:Curcumin