2.50
Hdl Handle:
http://hdl.handle.net/10033/345409
Title:
The green tea polyphenol, epigallocatechin-3-gallate, inhibits hepatitis C virus entry.
Authors:
Ciesek, Sandra; von Hahn, Thomas; Colpitts, Che C; Schang, Luis M; Friesland, Martina; Steinmann, Jörg; Manns, Michael P; Ott, Michael; Wedemeyer, Heiner; Meuleman, Philip; Pietschmann, Thomas; Steinmann, Eike
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.
Citation:
The green tea polyphenol, epigallocatechin-3-gallate, inhibits hepatitis C virus entry. 2011, 54 (6):1947-55 Hepatology
Journal:
Hepatology (Baltimore, Md.)
Issue Date:
Dec-2011
URI:
http://hdl.handle.net/10033/345409
DOI:
10.1002/hep.24610
PubMed ID:
21837753
Type:
Article
Language:
en
ISSN:
1527-3350
Appears in Collections:
publications of the department experimental Virology([TC]EVIR)

Full metadata record

DC FieldValue Language
dc.contributor.authorCiesek, Sandraen
dc.contributor.authorvon Hahn, Thomasen
dc.contributor.authorColpitts, Che Cen
dc.contributor.authorSchang, Luis Men
dc.contributor.authorFriesland, Martinaen
dc.contributor.authorSteinmann, Jörgen
dc.contributor.authorManns, Michael Pen
dc.contributor.authorOtt, Michaelen
dc.contributor.authorWedemeyer, Heineren
dc.contributor.authorMeuleman, Philipen
dc.contributor.authorPietschmann, Thomasen
dc.contributor.authorSteinmann, Eikeen
dc.date.accessioned2015-02-26T12:17:23Zen
dc.date.available2015-02-26T12:17:23Zen
dc.date.issued2011-12en
dc.identifier.citationThe green tea polyphenol, epigallocatechin-3-gallate, inhibits hepatitis C virus entry. 2011, 54 (6):1947-55 Hepatologyen
dc.identifier.issn1527-3350en
dc.identifier.pmid21837753en
dc.identifier.doi10.1002/hep.24610en
dc.identifier.urihttp://hdl.handle.net/10033/345409en
dc.description.abstractHepatitis 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.en
dc.language.isoenen
dc.subject.meshCatechinen
dc.subject.meshCell Line, Tumoren
dc.subject.meshCells, Cultureden
dc.subject.meshHepacivirusen
dc.subject.meshHepatitis Cen
dc.subject.meshHumansen
dc.subject.meshTeaen
dc.subject.meshVirus Attachmenten
dc.subject.meshVirus Internalizationen
dc.titleThe green tea polyphenol, epigallocatechin-3-gallate, inhibits hepatitis C virus entry.en
dc.typeArticleen
dc.identifier.journalHepatology (Baltimore, Md.)en

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