Curcumin inhibits hepatitis B virus via down-regulation of the metabolic coactivator PGC-1α

Maya Mouler Rechtman; Ofir Har-Noy; Iddo Bar-Yishay; Sigal Fishman; Yaarit Adamovich; Yosef Shaul; Zamir Halpern; Amir Shlomai

doi:10.1016/j.febslet.2010.04.067

Curcumin inhibits hepatitis B virus via down-regulation of the metabolic coactivator PGC-1α

Maya Mouler Rechtman, Ofir Har-Noy, Iddo Bar-Yishay, Sigal Fishman, Yaarit Adamovich, Yosef Shaul, Zamir Halpern, Amir Shlomai^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

110 Scopus citations

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-1α, 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.

Original language	English
Pages (from-to)	2485-2490
Number of pages	6
Journal	FEBS Letters
Volume	584
Issue number	11
DOIs	https://doi.org/10.1016/j.febslet.2010.04.067
State	Published - Jun 2010
Externally published	Yes

Funding

Funders	Funder number
Sackler Faculty of Medicine, Tel-Aviv University	2007285
Bloom's Syndrome Foundation
United States-Israel Binational Science Foundation

Keywords

Anti-viral therapy
Hepatitis B virus
Metabolovirus
Nutrition

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.febslet.2010.04.067

Cite this

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title = "Curcumin inhibits hepatitis B virus via down-regulation of the metabolic coactivator PGC-1α",

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-1α, 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.",

keywords = "Anti-viral therapy, Hepatitis B virus, Metabolovirus, Nutrition",

author = "\{Mouler Rechtman\}, Maya and Ofir Har-Noy and Iddo Bar-Yishay and Sigal Fishman and Yaarit Adamovich and Yosef Shaul and Zamir Halpern and Amir Shlomai",

note = "Funding Information: This work was supported by the following Grants: Schraiber Grant from the Sackler faculty of Medicine, Tel-Aviv University, The Weizmann–Ichilov Joint Grant and Grant No. 2007285 from the United States-Israel Binational Science Foundation (BSF) .",

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AU - Mouler Rechtman, Maya

AU - Har-Noy, Ofir

AU - Bar-Yishay, Iddo

AU - Fishman, Sigal

AU - Adamovich, Yaarit

AU - Shaul, Yosef

AU - Halpern, Zamir

AU - Shlomai, Amir

N1 - Funding Information: This work was supported by the following Grants: Schraiber Grant from the Sackler faculty of Medicine, Tel-Aviv University, The Weizmann–Ichilov Joint Grant and Grant No. 2007285 from the United States-Israel Binational Science Foundation (BSF) .

PY - 2010/6

Y1 - 2010/6

N2 - 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-1α, 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.

AB - 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-1α, 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.

KW - Anti-viral therapy

KW - Hepatitis B virus

KW - Metabolovirus

KW - Nutrition

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ER -

Curcumin inhibits hepatitis B virus via down-regulation of the metabolic coactivator PGC-1α

Abstract

Funding

Keywords

UN SDGs

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