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Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection.

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Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection. / Protzer, Ulrike; Seyfried, Stefan; Quasdorff, Maria; Sass, Gabriele; Svorcova, Miriam; Webb, Dennis; Bohne, Felix; Hösel, Marianna; Schirmacher, Peter; Tiegs, Gisa.

In: GASTROENTEROLOGY, Vol. 133, No. 4, 4, 2007, p. 1156-1165.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Protzer, U, Seyfried, S, Quasdorff, M, Sass, G, Svorcova, M, Webb, D, Bohne, F, Hösel, M, Schirmacher, P & Tiegs, G 2007, 'Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection.', GASTROENTEROLOGY, vol. 133, no. 4, 4, pp. 1156-1165. <http://www.ncbi.nlm.nih.gov/pubmed/17919491?dopt=Citation>

APA

Protzer, U., Seyfried, S., Quasdorff, M., Sass, G., Svorcova, M., Webb, D., Bohne, F., Hösel, M., Schirmacher, P., & Tiegs, G. (2007). Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection. GASTROENTEROLOGY, 133(4), 1156-1165. [4]. http://www.ncbi.nlm.nih.gov/pubmed/17919491?dopt=Citation

Vancouver

Protzer U, Seyfried S, Quasdorff M, Sass G, Svorcova M, Webb D et al. Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection. GASTROENTEROLOGY. 2007;133(4):1156-1165. 4.

Bibtex

@article{290c3f8157344de88c177a4aa61ccd89,
title = "Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection.",
abstract = "BACKGROUND ; AIMS: Induction of heme oxygenase-1 (HO-1) has been shown to be beneficial in immune-mediated liver damage. We now investigate the effects of HO-1 induction in models of human hepatitis B virus (HBV) infection. METHODS: Adenoviral transfer of an HBV 1.3 genome into wild-type mice was used as a model for acute hepatitis B. HBV transgenic animals were used as a model for chronic HBV infection. HBV replication was assessed by HBV viremia, antigenemia, and Southern blotting, liver damage was assessed by serum alanine aminotransferase activities and histopathology of liver sections. To investigate HO-1 effects on HBV replication at a molecular level, stably HBV-transfected hepatoma cells were used. HBV gene expression, protein stability, transcription, and replication were determined. HO-1 was induced by either cobalt-protoporphyrin-IX or over expressed by adenoviral gene transfer. RESULTS: In the acute hepatitis B model, liver injury was reduced significantly after HO-1 induction. In addition, HO-1 showed a pronounced antiviral effect, which was confirmed in stably HBV-transfected hepatoma cells and in persistently HBV replicating transgenic mice. We showed that HO-1 induction repressed HBV replication directly in hepatocytes at a posttranscriptional step by reducing stability of HBV core protein and thus blocking refill of nuclear HBV covalently closed circular (ccc)DNA. Small interfering RNA directed against HO-1 proved that this effect depended on the expression level of HO-1. CONCLUSIONS: Besides its hepatoprotective effect, HO-1 showed a pronounced antiviral activity in HBV infection. Therefore, induction of HO-1 might be a novel therapeutic option for inflammatory flares of hepatitis B.",
author = "Ulrike Protzer and Stefan Seyfried and Maria Quasdorff and Gabriele Sass and Miriam Svorcova and Dennis Webb and Felix Bohne and Marianna H{\"o}sel and Peter Schirmacher and Gisa Tiegs",
year = "2007",
language = "Deutsch",
volume = "133",
pages = "1156--1165",
journal = "GASTROENTEROLOGY",
issn = "0016-5085",
publisher = "W.B. Saunders Ltd",
number = "4",

}

RIS

TY - JOUR

T1 - Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection.

AU - Protzer, Ulrike

AU - Seyfried, Stefan

AU - Quasdorff, Maria

AU - Sass, Gabriele

AU - Svorcova, Miriam

AU - Webb, Dennis

AU - Bohne, Felix

AU - Hösel, Marianna

AU - Schirmacher, Peter

AU - Tiegs, Gisa

PY - 2007

Y1 - 2007

N2 - BACKGROUND ; AIMS: Induction of heme oxygenase-1 (HO-1) has been shown to be beneficial in immune-mediated liver damage. We now investigate the effects of HO-1 induction in models of human hepatitis B virus (HBV) infection. METHODS: Adenoviral transfer of an HBV 1.3 genome into wild-type mice was used as a model for acute hepatitis B. HBV transgenic animals were used as a model for chronic HBV infection. HBV replication was assessed by HBV viremia, antigenemia, and Southern blotting, liver damage was assessed by serum alanine aminotransferase activities and histopathology of liver sections. To investigate HO-1 effects on HBV replication at a molecular level, stably HBV-transfected hepatoma cells were used. HBV gene expression, protein stability, transcription, and replication were determined. HO-1 was induced by either cobalt-protoporphyrin-IX or over expressed by adenoviral gene transfer. RESULTS: In the acute hepatitis B model, liver injury was reduced significantly after HO-1 induction. In addition, HO-1 showed a pronounced antiviral effect, which was confirmed in stably HBV-transfected hepatoma cells and in persistently HBV replicating transgenic mice. We showed that HO-1 induction repressed HBV replication directly in hepatocytes at a posttranscriptional step by reducing stability of HBV core protein and thus blocking refill of nuclear HBV covalently closed circular (ccc)DNA. Small interfering RNA directed against HO-1 proved that this effect depended on the expression level of HO-1. CONCLUSIONS: Besides its hepatoprotective effect, HO-1 showed a pronounced antiviral activity in HBV infection. Therefore, induction of HO-1 might be a novel therapeutic option for inflammatory flares of hepatitis B.

AB - BACKGROUND ; AIMS: Induction of heme oxygenase-1 (HO-1) has been shown to be beneficial in immune-mediated liver damage. We now investigate the effects of HO-1 induction in models of human hepatitis B virus (HBV) infection. METHODS: Adenoviral transfer of an HBV 1.3 genome into wild-type mice was used as a model for acute hepatitis B. HBV transgenic animals were used as a model for chronic HBV infection. HBV replication was assessed by HBV viremia, antigenemia, and Southern blotting, liver damage was assessed by serum alanine aminotransferase activities and histopathology of liver sections. To investigate HO-1 effects on HBV replication at a molecular level, stably HBV-transfected hepatoma cells were used. HBV gene expression, protein stability, transcription, and replication were determined. HO-1 was induced by either cobalt-protoporphyrin-IX or over expressed by adenoviral gene transfer. RESULTS: In the acute hepatitis B model, liver injury was reduced significantly after HO-1 induction. In addition, HO-1 showed a pronounced antiviral effect, which was confirmed in stably HBV-transfected hepatoma cells and in persistently HBV replicating transgenic mice. We showed that HO-1 induction repressed HBV replication directly in hepatocytes at a posttranscriptional step by reducing stability of HBV core protein and thus blocking refill of nuclear HBV covalently closed circular (ccc)DNA. Small interfering RNA directed against HO-1 proved that this effect depended on the expression level of HO-1. CONCLUSIONS: Besides its hepatoprotective effect, HO-1 showed a pronounced antiviral activity in HBV infection. Therefore, induction of HO-1 might be a novel therapeutic option for inflammatory flares of hepatitis B.

M3 - SCORING: Zeitschriftenaufsatz

VL - 133

SP - 1156

EP - 1165

JO - GASTROENTEROLOGY

JF - GASTROENTEROLOGY

SN - 0016-5085

IS - 4

M1 - 4

ER -