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dc.contributor.authorBruening, Janina
dc.contributor.authorWeigel, Bettina
dc.contributor.authorGerold, Gisa
dc.date.accessioned2018-01-09T15:25:20Z
dc.date.available2018-01-09T15:25:20Z
dc.date.issued2017
dc.identifier.citationThe Role of Type III Interferons in Hepatitis C Virus Infection and Therapy. 2017, 2017:7232361 J Immunol Resen
dc.identifier.issn2314-7156
dc.identifier.pmid28255563
dc.identifier.doi10.1155/2017/7232361
dc.identifier.urihttp://hdl.handle.net/10033/621229
dc.description.abstractThe human interferon (IFN) response is a key innate immune mechanism to fight virus infection. IFNs are host-encoded secreted proteins, which induce IFN-stimulated genes (ISGs) with antiviral properties. Among the three classes of IFNs, type III IFNs, also called IFN lambdas (IFNLs), are an essential component of the innate immune response to hepatitis C virus (HCV). In particular, human polymorphisms in IFNL gene loci correlate with hepatitis C disease progression and with treatment response. To date, the underlying mechanisms remain mostly elusive; however it seems clear that viral infection of the liver induces IFNL responses. As IFNL receptors show a more restricted tissue expression than receptors for other classes of IFNs, IFNL treatment has reduced side effects compared to the classical type I IFN treatment. In HCV therapy, however, IFNL will likely not play an important role as highly effective direct acting antivirals (DAA) exist. Here, we will review our current knowledge on IFNL gene expression, protein properties, signaling, ISG induction, and its implications on HCV infection and treatment. Finally, we will discuss the lessons learnt from the HCV and IFNL field for virus infections beyond hepatitis C.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAnimalsen
dc.subject.meshAntiviral Agentsen
dc.subject.meshHepacivirusen
dc.subject.meshHepatitis Cen
dc.subject.meshHost-Pathogen Interactionsen
dc.subject.meshHumansen
dc.subject.meshImmunity, Innateen
dc.subject.meshInterferonsen
dc.subject.meshInterleukinsen
dc.subject.meshLiveren
dc.subject.meshSignal Transductionen
dc.subject.meshVirus Replicationen
dc.titleThe Role of Type III Interferons in Hepatitis C Virus Infection and Therapy.en
dc.typeArticleen
dc.contributor.departmentTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH, Feodor-Lynen-Str. 7, 30625 Hannover, Germany.en
dc.identifier.journalJournal of immunology researchen
refterms.dateFOA2018-06-12T16:43:11Z
html.description.abstractThe human interferon (IFN) response is a key innate immune mechanism to fight virus infection. IFNs are host-encoded secreted proteins, which induce IFN-stimulated genes (ISGs) with antiviral properties. Among the three classes of IFNs, type III IFNs, also called IFN lambdas (IFNLs), are an essential component of the innate immune response to hepatitis C virus (HCV). In particular, human polymorphisms in IFNL gene loci correlate with hepatitis C disease progression and with treatment response. To date, the underlying mechanisms remain mostly elusive; however it seems clear that viral infection of the liver induces IFNL responses. As IFNL receptors show a more restricted tissue expression than receptors for other classes of IFNs, IFNL treatment has reduced side effects compared to the classical type I IFN treatment. In HCV therapy, however, IFNL will likely not play an important role as highly effective direct acting antivirals (DAA) exist. Here, we will review our current knowledge on IFNL gene expression, protein properties, signaling, ISG induction, and its implications on HCV infection and treatment. Finally, we will discuss the lessons learnt from the HCV and IFNL field for virus infections beyond hepatitis C.


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