2.50
Hdl Handle:
http://hdl.handle.net/10033/325483
Title:
Molecular basis of interferon resistance in hepatitis C virus.
Authors:
Perales, Celia; Beach, Nathan M; Sheldon, Julie; Domingo, Esteban
Abstract:
Resistance to interferon (IFN) in hepatitis C virus (HCV) differs from resistance to standard, directly-acting antiviral (DAA) agents in that the virus confronts a multicomponent antiviral state evoked by IFN. This renders unlikely the repeated selection of the same specific mutations that confer an IFN-resistance phenotype. Comparison of amino acid sequences of viral proteins in HCV that replicates in the presence of IFN in vivo or in cell culture (with entire virus or subgenomic replicons) reveals very few common candidate IFN resistance substitutions. Multiple host and viral factors contribute to divergent responses to IFN. The environmental heterogeneity in which exogenous IFN is expected to exert its selective effect may increase as a result of incorporation of new DAAs in therapy.
Citation:
Molecular basis of interferon resistance in hepatitis C virus. 2014, 8C:38-44 Curr Opin Virol
Journal:
Current opinion in virology
Issue Date:
23-Jun-2014
URI:
http://hdl.handle.net/10033/325483
DOI:
10.1016/j.coviro.2014.05.003
PubMed ID:
24968186
Type:
Article
ISSN:
1879-6265
Appears in Collections:
publications of the department experimental Virology([TC]EVIR)

Full metadata record

DC FieldValue Language
dc.contributor.authorPerales, Celiaen
dc.contributor.authorBeach, Nathan Men
dc.contributor.authorSheldon, Julieen
dc.contributor.authorDomingo, Estebanen
dc.date.accessioned2014-08-27T12:51:47Z-
dc.date.available2014-08-27T12:51:47Z-
dc.date.issued2014-06-23-
dc.identifier.citationMolecular basis of interferon resistance in hepatitis C virus. 2014, 8C:38-44 Curr Opin Virolen
dc.identifier.issn1879-6265-
dc.identifier.pmid24968186-
dc.identifier.doi10.1016/j.coviro.2014.05.003-
dc.identifier.urihttp://hdl.handle.net/10033/325483-
dc.description.abstractResistance to interferon (IFN) in hepatitis C virus (HCV) differs from resistance to standard, directly-acting antiviral (DAA) agents in that the virus confronts a multicomponent antiviral state evoked by IFN. This renders unlikely the repeated selection of the same specific mutations that confer an IFN-resistance phenotype. Comparison of amino acid sequences of viral proteins in HCV that replicates in the presence of IFN in vivo or in cell culture (with entire virus or subgenomic replicons) reveals very few common candidate IFN resistance substitutions. Multiple host and viral factors contribute to divergent responses to IFN. The environmental heterogeneity in which exogenous IFN is expected to exert its selective effect may increase as a result of incorporation of new DAAs in therapy.en
dc.languageENG-
dc.rightsArchived with thanks to Current opinion in virologyen
dc.titleMolecular basis of interferon resistance in hepatitis C virus.-
dc.typeArticleen
dc.identifier.journalCurrent opinion in virologyen

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