Hepatocyte metabolic signalling pathways and regulation of hepatitis B virus expression

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2010.02423.x/abstract

Hepatocyte metabolic signalling pathways and regulation of hepatitis B virus

expression

Iddo Bar-Yishay1, Yosef Shaul2, Amir Shlomai1Article first published online: 11

JAN 2011

DOI: 10.1111/j.1478-3231.2010.02423.x

© 2011 Wiley & Sons A/S

Issue

Liver International

Early View (Articles online in advance of print)

Abstract

Hepatitis B virus (HBV) is a small DNA virus responsible for significant

morbidity and mortality worldwide. The liver, which is the main target organ for

HBV infection, provides the virus with the machinery necessary for persistent

infection and propagation, a process that might ultimately lead to severe liver

pathologies such as chronic hepatitis, cirrhosis and liver cancer. HBV gene

expression is regulated mainly at the transcriptional level by recruitment of a

whole set of cellular transcription factors (TFs) and co-activators to support

transcription. Over the years, many of these TFs were identified and

interestingly enough most are associated with the body's nutritional state.

These include the hepatocyte nuclear factors, forkhead Box O1, Farnesoid X

receptor, cyclic-AMP response element-binding (CREB), CCAAT/enhancer-binding

protein (C/EBP) and glucocorticoid receptor TFs and the transcription

coactivator PPARã coactivator-1á. Consequently, HBV gene expression is linked to

hepatic metabolic processes such as glucose and fat production and utilization

as well as bile acids' production and secretion. Furthermore, recent evidence

indicates that HBV actively interferes with some of these hepatic metabolic

processes by manipulating key TFs, such as CREB and C/EBP, to meet its

requirements. The discovery of the mechanisms by which HBV is controlled by the

hepatic metabolic milieu may broaden our understanding of the unique regulation

of HBV expression and may also explain the mechanisms by which HBV induces liver

pathologies. The emerging principle of the intimate link between HBV and liver

metabolism can be further exploited for host-targeted therapeutic strategies.

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2010.02423.x/abstract

Hepatocyte metabolic signalling pathways and regulation of hepatitis B virus

expression

Iddo Bar-Yishay1, Yosef Shaul2, Amir Shlomai1Article first published online: 11

JAN 2011

DOI: 10.1111/j.1478-3231.2010.02423.x

© 2011 Wiley & Sons A/S

Issue

Liver International

Early View (Articles online in advance of print)

Abstract

Hepatitis B virus (HBV) is a small DNA virus responsible for significant

morbidity and mortality worldwide. The liver, which is the main target organ for

HBV infection, provides the virus with the machinery necessary for persistent

infection and propagation, a process that might ultimately lead to severe liver

pathologies such as chronic hepatitis, cirrhosis and liver cancer. HBV gene

expression is regulated mainly at the transcriptional level by recruitment of a

whole set of cellular transcription factors (TFs) and co-activators to support

transcription. Over the years, many of these TFs were identified and

interestingly enough most are associated with the body's nutritional state.

These include the hepatocyte nuclear factors, forkhead Box O1, Farnesoid X

receptor, cyclic-AMP response element-binding (CREB), CCAAT/enhancer-binding

protein (C/EBP) and glucocorticoid receptor TFs and the transcription

coactivator PPARã coactivator-1á. Consequently, HBV gene expression is linked to

hepatic metabolic processes such as glucose and fat production and utilization

as well as bile acids' production and secretion. Furthermore, recent evidence

indicates that HBV actively interferes with some of these hepatic metabolic

processes by manipulating key TFs, such as CREB and C/EBP, to meet its

requirements. The discovery of the mechanisms by which HBV is controlled by the

hepatic metabolic milieu may broaden our understanding of the unique regulation

of HBV expression and may also explain the mechanisms by which HBV induces liver

pathologies. The emerging principle of the intimate link between HBV and liver

metabolism can be further exploited for host-targeted therapeutic strategies.

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2010.02423.x/abstract

Hepatocyte metabolic signalling pathways and regulation of hepatitis B virus

expression

Iddo Bar-Yishay1, Yosef Shaul2, Amir Shlomai1Article first published online: 11

JAN 2011

DOI: 10.1111/j.1478-3231.2010.02423.x

© 2011 Wiley & Sons A/S

Issue

Liver International

Early View (Articles online in advance of print)

Abstract

Hepatitis B virus (HBV) is a small DNA virus responsible for significant

morbidity and mortality worldwide. The liver, which is the main target organ for

HBV infection, provides the virus with the machinery necessary for persistent

infection and propagation, a process that might ultimately lead to severe liver

pathologies such as chronic hepatitis, cirrhosis and liver cancer. HBV gene

expression is regulated mainly at the transcriptional level by recruitment of a

whole set of cellular transcription factors (TFs) and co-activators to support

transcription. Over the years, many of these TFs were identified and

interestingly enough most are associated with the body's nutritional state.

These include the hepatocyte nuclear factors, forkhead Box O1, Farnesoid X

receptor, cyclic-AMP response element-binding (CREB), CCAAT/enhancer-binding

protein (C/EBP) and glucocorticoid receptor TFs and the transcription

coactivator PPARã coactivator-1á. Consequently, HBV gene expression is linked to

hepatic metabolic processes such as glucose and fat production and utilization

as well as bile acids' production and secretion. Furthermore, recent evidence

indicates that HBV actively interferes with some of these hepatic metabolic

processes by manipulating key TFs, such as CREB and C/EBP, to meet its

requirements. The discovery of the mechanisms by which HBV is controlled by the

hepatic metabolic milieu may broaden our understanding of the unique regulation

of HBV expression and may also explain the mechanisms by which HBV induces liver

pathologies. The emerging principle of the intimate link between HBV and liver

metabolism can be further exploited for host-targeted therapeutic strategies.

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2010.02423.x/abstract

Hepatocyte metabolic signalling pathways and regulation of hepatitis B virus

expression

Iddo Bar-Yishay1, Yosef Shaul2, Amir Shlomai1Article first published online: 11

JAN 2011

DOI: 10.1111/j.1478-3231.2010.02423.x

© 2011 Wiley & Sons A/S

Issue

Liver International

Early View (Articles online in advance of print)

Abstract

Hepatitis B virus (HBV) is a small DNA virus responsible for significant

morbidity and mortality worldwide. The liver, which is the main target organ for

HBV infection, provides the virus with the machinery necessary for persistent

infection and propagation, a process that might ultimately lead to severe liver

pathologies such as chronic hepatitis, cirrhosis and liver cancer. HBV gene

expression is regulated mainly at the transcriptional level by recruitment of a

whole set of cellular transcription factors (TFs) and co-activators to support

transcription. Over the years, many of these TFs were identified and

interestingly enough most are associated with the body's nutritional state.

These include the hepatocyte nuclear factors, forkhead Box O1, Farnesoid X

receptor, cyclic-AMP response element-binding (CREB), CCAAT/enhancer-binding

protein (C/EBP) and glucocorticoid receptor TFs and the transcription

coactivator PPARã coactivator-1á. Consequently, HBV gene expression is linked to

hepatic metabolic processes such as glucose and fat production and utilization

as well as bile acids' production and secretion. Furthermore, recent evidence

indicates that HBV actively interferes with some of these hepatic metabolic

processes by manipulating key TFs, such as CREB and C/EBP, to meet its

requirements. The discovery of the mechanisms by which HBV is controlled by the

hepatic metabolic milieu may broaden our understanding of the unique regulation

of HBV expression and may also explain the mechanisms by which HBV induces liver

pathologies. The emerging principle of the intimate link between HBV and liver

metabolism can be further exploited for host-targeted therapeutic strategies.