The green tea polyphenol, epigallocatechin‐3‐gallate, inhibits hepatitis C virus entry
Hepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a substantial proportion of cases. Drug development is focused on nonstructural proteins required for RNA replication. Individuals undergoing orthotopic liv...
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Published in | Hepatology (Baltimore, Md.) Vol. 54; no. 6; pp. 1947 - 1955 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.12.2011
Wiley Wiley Subscription Services, Inc |
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Abstract | Hepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a substantial proportion of cases. Drug development is focused on nonstructural proteins required for RNA replication. Individuals undergoing orthotopic liver transplantation face rapid, universal reinfection of the graft. Therefore, antiviral strategies targeting the early stages of infection are urgently needed for the prevention of HCV infection. In this study, we identified the polyphenol, epigallocatechin‐3‐gallate (EGCG), as an inhibitor of HCV entry. Green tea catechins, such as EGCG and its derivatives, epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC), have been previously found to exert antiviral and antioncogenic properties. EGCG had no effect on HCV RNA replication, assembly, or release of progeny virions. However, it potently inhibited Cell‐culture–derived HCV (HCVcc) entry into hepatoma cell lines as well as primary human hepatocytes. The effect was independent of the HCV genotype, and both infection of cells by extracellular virions and cell‐to‐cell spread were blocked. Pretreatment of cells with EGCG before HCV inoculation did not reduce HCV infection, whereas the application of EGCG during inoculation strongly inhibited HCV infectivity. Moreover, treatment with EGCG directly during inoculation strongly inhibited HCV infectivity. Expression levels of all known HCV (co‐)receptors were unaltered by EGCG. Finally, we showed that EGCG inhibits viral attachment to the cell, thus disrupting the initial step of HCV cell entry. Conclusion: The green tea molecule, EGCG, potently inhibits HCV entry and could be part of an antiviral strategy aimed at the prevention of HCV reinfection after liver transplantation. (HEPATOLOGY 2011) |
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AbstractList | UNLABELLEDHepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a substantial proportion of cases. Drug development is focused on nonstructural proteins required for RNA replication. Individuals undergoing orthotopic liver transplantation face rapid, universal reinfection of the graft. Therefore, antiviral strategies targeting the early stages of infection are urgently needed for the prevention of HCV infection. In this study, we identified the polyphenol, epigallocatechin-3-gallate (EGCG), as an inhibitor of HCV entry. Green tea catechins, such as EGCG and its derivatives, epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC), have been previously found to exert antiviral and antioncogenic properties. EGCG had no effect on HCV RNA replication, assembly, or release of progeny virions. However, it potently inhibited Cell-culture-derived HCV (HCVcc) entry into hepatoma cell lines as well as primary human hepatocytes. The effect was independent of the HCV genotype, and both infection of cells by extracellular virions and cell-to-cell spread were blocked. Pretreatment of cells with EGCG before HCV inoculation did not reduce HCV infection, whereas the application of EGCG during inoculation strongly inhibited HCV infectivity. Moreover, treatment with EGCG directly during inoculation strongly inhibited HCV infectivity. Expression levels of all known HCV (co-)receptors were unaltered by EGCG. Finally, we showed that EGCG inhibits viral attachment to the cell, thus disrupting the initial step of HCV cell entry.CONCLUSIONThe green tea molecule, EGCG, potently inhibits HCV entry and could be part of an antiviral strategy aimed at the prevention of HCV reinfection after liver transplantation. Hepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a substantial proportion of cases. Drug development is focused on nonstructural proteins required for RNA replication. Individuals undergoing orthotopic liver transplantation face rapid, universal reinfection of the graft. Therefore, antiviral strategies targeting the early stages of infection are urgently needed for the prevention of HCV infection. In this study, we identified the polyphenol, epigallocatechin-3-gallate (EGCG), as an inhibitor of HCV entry. Green tea catechins, such as EGCG and its derivatives, epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC), have been previously found to exert antiviral and antioncogenic properties. EGCG had no effect on HCV RNA replication, assembly, or release of progeny virions. However, it potently inhibited Cell-culture-derived HCV (HCVcc) entry into hepatoma cell lines as well as primary human hepatocytes. The effect was independent of the HCV genotype, and both infection of cells by extracellular virions and cell-to-cell spread were blocked. Pretreatment of cells with EGCG before HCV inoculation did not reduce HCV infection, whereas the application of EGCG during inoculation strongly inhibited HCV infectivity. Moreover, treatment with EGCG directly during inoculation strongly inhibited HCV infectivity. Expression levels of all known HCV (co-)receptors were unaltered by EGCG. Finally, we showed that EGCG inhibits viral attachment to the cell, thus disrupting the initial step of HCV cell entry. Conclusion: The green tea molecule, EGCG, potently inhibits HCV entry and could be part of an antiviral strategy aimed at the prevention of HCV reinfection after liver transplantation. (HEPATOLOGY 2011) Hepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a substantial proportion of cases. Drug development is focused on nonstructural proteins required for RNA replication. Individuals undergoing orthotopic liver transplantation face rapid, universal reinfection of the graft. Therefore, antiviral strategies targeting the early stages of infection are urgently needed for the prevention of HCV infection. In this study, we identified the polyphenol, epigallocatechin-3-gallate (EGCG), as an inhibitor of HCV entry. Green tea catechins, such as EGCG and its derivatives, epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC), have been previously found to exert antiviral and antioncogenic properties. EGCG had no effect on HCV RNA replication, assembly, or release of progeny virions. However, it potently inhibited Cell-culture-derived HCV (HCVcc) entry into hepatoma cell lines as well as primary human hepatocytes. The effect was independent of the HCV genotype, and both infection of cells by extracellular virions and cell-to-cell spread were blocked. Pretreatment of cells with EGCG before HCV inoculation did not reduce HCV infection, whereas the application of EGCG during inoculation strongly inhibited HCV infectivity. Moreover, treatment with EGCG directly during inoculation strongly inhibited HCV infectivity. Expression levels of all known HCV (co-)receptors were unaltered by EGCG. Finally, we showed that EGCG inhibits viral attachment to the cell, thus disrupting the initial step of HCV cell entry. The green tea molecule, EGCG, potently inhibits HCV entry and could be part of an antiviral strategy aimed at the prevention of HCV reinfection after liver transplantation. |
Author | Schang, Luis M. Wedemeyer, Heiner Ciesek, Sandra Colpitts, Che C. Steinmann, Jörg Ott, Michael Friesland, Martina von Hahn, Thomas Meuleman, Philip Manns, Michael P. Steinmann, Eike Pietschmann, Thomas |
Author_xml | – sequence: 1 givenname: Sandra surname: Ciesek fullname: Ciesek, Sandra email: ciesek.sandra@mh‐hannover.de – sequence: 2 givenname: Thomas surname: von Hahn fullname: von Hahn, Thomas – sequence: 3 givenname: Che C. surname: Colpitts fullname: Colpitts, Che C. – sequence: 4 givenname: Luis M. surname: Schang fullname: Schang, Luis M. – sequence: 5 givenname: Martina surname: Friesland fullname: Friesland, Martina – sequence: 6 givenname: Jörg surname: Steinmann fullname: Steinmann, Jörg – sequence: 7 givenname: Michael P. surname: Manns fullname: Manns, Michael P. – sequence: 8 givenname: Michael surname: Ott fullname: Ott, Michael – sequence: 9 givenname: Heiner surname: Wedemeyer fullname: Wedemeyer, Heiner – sequence: 10 givenname: Philip surname: Meuleman fullname: Meuleman, Philip – sequence: 11 givenname: Thomas surname: Pietschmann fullname: Pietschmann, Thomas – sequence: 12 givenname: Eike surname: Steinmann fullname: Steinmann, Eike |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25339789$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21837753$$D View this record in MEDLINE/PubMed |
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Copyright | Copyright © 2011 American Association for the Study of Liver Diseases 2015 INIST-CNRS Copyright © 2011 American Association for the Study of Liver Diseases. |
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Keywords | Virus Polyphenol Gastroenterology Phenols Flaviviridae Hepatitis C virus Hepacivirus Green tea |
Language | English |
License | CC BY 4.0 Copyright © 2011 American Association for the Study of Liver Diseases. |
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Notes | Potential conflict of interest: Dr. Schang is a consultant for Epiphany Biosciences. fax: +49 511 220027186 This work was supported by grants from the Deutsche Forschungsgemeinschaft (DFG) (HA 4393/2‐1; to T.V.H.) and (Ci 171/2‐1; to S.C.) and from the CIHR and BWF (to L.M.S.). T.P. was supported by grants from the Helmholtz Association SO‐024 and the DFG (PI 734/2‐1 and SFB 900, Teilprojekt A6). E.S. was supported by an intramural young investigator award of the Helmholtz Center for Infection Research and the DFG (STE 1954/1‐1). C.C.C. was supported by the NSERC and AHFMR. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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Hepatol doi: 10.1016/j.jhep.2010.10.014 contributor: fullname: Zeisel – volume: 28 start-page: 167 year: 2010 ident: 10.1002/hep.24610-BIB19|cit19 article-title: Real-time imaging of hepatitis C virus infection using a fluorescent cell-based reporter system publication-title: Nat Biotechnol doi: 10.1038/nbt.1604 contributor: fullname: Jones – volume: 281 start-page: 25177 year: 2006 ident: 10.1002/hep.24610-BIB21|cit21 article-title: Cyanovirin-N inhibits hepatitis C virus entry by binding to envelope protein glycans publication-title: J Biol Chem doi: 10.1074/jbc.M602431200 contributor: fullname: Helle – volume: 11 start-page: 791 year: 2005 ident: 10.1002/hep.24610-BIB5|cit5 article-title: Production of infectious hepatitis C virus in tissue culture from a cloned viral genome publication-title: Nat Med doi: 10.1038/nm1268 contributor: fullname: Wakita – volume: 138 start-page: 1875 year: 2010 ident: 10.1002/hep.24610-BIB4|cit4 article-title: Glucocorticosteroids increase cell entry 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Nat Med doi: 10.1038/nm.2341 contributor: fullname: Lupberger – volume: 85 start-page: 7613 year: 2011 ident: 10.1002/hep.24610-BIB18|cit18 article-title: Impact of occludin intra- and interspecies variation on its coreceptor function for authentic hepatitis C virus particles publication-title: J Virol doi: 10.1128/JVI.00212-11 contributor: fullname: Ciesek – volume: 76 start-page: 86 year: 2007 ident: 10.1002/hep.24610-BIB28|cit28 article-title: Activity of compounds from Chinese herbal medicine Rhodiola kirilowii (Regel) Maxim against HCV NS3 serine protease publication-title: Antiviral Res doi: 10.1016/j.antiviral.2007.06.001 contributor: fullname: Zuo – volume: 102 start-page: 9294 year: 2005 ident: 10.1002/hep.24610-BIB7|cit7 article-title: Robust hepatitis C virus infection in vitro publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0503596102 contributor: fullname: Zhong – volume: 58 start-page: 167 year: 2003 ident: 10.1002/hep.24610-BIB11|cit11 article-title: 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Snippet | Hepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a substantial... UNLABELLEDHepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a... |
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SubjectTerms | Biological and medical sciences Catechin - analogs & derivatives Catechin - pharmacology Cell Line, Tumor Cells, Cultured Gastroenterology. Liver. Pancreas. Abdomen Hepacivirus - drug effects Hepacivirus - physiology Hepatitis Hepatitis C Hepatitis C - prevention & control Hepatitis C virus Hepatology Humans Liver cirrhosis Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences Tea Tea - chemistry Transplants & implants Virus Attachment - drug effects Virus Internalization - drug effects |
Title | The green tea polyphenol, epigallocatechin‐3‐gallate, inhibits hepatitis C virus entry |
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