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Hepatitis C virus replication in mouse cells is restricted by IFN-dependent and -independent mechanisms.
Nandakumar, Ramya Finsterbusch, Katja Lipps, Christoph Neumann, Berit Grashoff, Martina Nair, Sharmila Hochnadel, Inga Lienenklaus, Stefan Wappler, Ilka Steinmann, Eike
Nandakumar, Ramya
Finsterbusch, Katja
Lipps, Christoph
Neumann, Berit
Grashoff, Martina
Nair, Sharmila
Hochnadel, Inga
Lienenklaus, Stefan
Wappler, Ilka
Steinmann, Eike
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2013-12
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Current 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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Hepatitis C virus replication in mouse cells is restricted by IFN-dependent and -independent mechanisms. 2013, 145 (6):1414-23.e1 Gastroenterology
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en
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1528-0012
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