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dc.contributor.authorNandakumar, Ramya
dc.contributor.authorFinsterbusch, Katja
dc.contributor.authorLipps, Christoph
dc.contributor.authorNeumann, Berit
dc.contributor.authorGrashoff, Martina
dc.contributor.authorNair, Sharmila
dc.contributor.authorHochnadel, Inga
dc.contributor.authorLienenklaus, Stefan
dc.contributor.authorWappler, Ilka
dc.contributor.authorSteinmann, Eike
dc.contributor.authorHauser, Hansjörg
dc.contributor.authorPietschmann, Thomas
dc.contributor.authorKröger, Andrea
dc.date.accessioned2014-01-16T15:27:18Zen
dc.date.available2014-01-16T15:27:18Zen
dc.date.issued2013-12en
dc.identifier.citationHepatitis C virus replication in mouse cells is restricted by IFN-dependent and -independent mechanisms. 2013, 145 (6):1414-23.e1 Gastroenterologyen
dc.identifier.issn1528-0012en
dc.identifier.pmid23973921en
dc.identifier.doi10.1053/j.gastro.2013.08.037en
dc.identifier.urihttp://hdl.handle.net/10033/311411en
dc.description.abstractCurrent treatment strategies for hepatitis C virus (HCV) infection include pegylated interferon (IFN)-alfa and ribavirin. Approximately 50% of patients control HCV infection after treatment, but the broad range of patients' outcomes and responses to treatment, among all genotypes, indicates a role for host factors. Although the IFN system is important in limiting HCV replication, the virus has evolved mechanisms to circumvent the IFN response. However, direct, IFN-independent antiviral processes also might help control HCV replication. We examined the role of IFN-independent responses against HCV replication.
dc.language.isoenen
dc.rightsArchived with thanks to Gastroenterologyen
dc.titleHepatitis C virus replication in mouse cells is restricted by IFN-dependent and -independent mechanisms.en
dc.typeArticleen
dc.contributor.departmentHelmholtz Centre for infection research, D38124 Braunschweig, Germanyen
dc.identifier.journalGastroenterologyen
refterms.dateFOA2018-06-13T09:08:20Z
html.description.abstractCurrent treatment strategies for hepatitis C virus (HCV) infection include pegylated interferon (IFN)-alfa and ribavirin. Approximately 50% of patients control HCV infection after treatment, but the broad range of patients' outcomes and responses to treatment, among all genotypes, indicates a role for host factors. Although the IFN system is important in limiting HCV replication, the virus has evolved mechanisms to circumvent the IFN response. However, direct, IFN-independent antiviral processes also might help control HCV replication. We examined the role of IFN-independent responses against HCV replication.


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