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Virologic relapse after treatment can occur, and in some studies was more common in cirrhotic subjects. We previously observed changes in hepatic immunity during interferon (IFN)\u2010free therapy that correlated with favourable outcome in subjects with early liver disease. Here, we compared changes in endogenous IFN pathways during IFN\u2010free, RBV\u2010free therapy between cirrhotic and noncirrhotic subjects. <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> (miRNA) expression analyses were performed on paired pre\u2010 and post\u2010treatment liver biopsies from genotype\u20101 <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> subjects treated with sofosbuvir\/ledipasvir (SOF\/LDV) for 12 weeks (<jats:italic>n<\/jats:italic> = 4, 3 cirrhotics) or SOF\/LDV combined with <jats:styled-content style=\"fixed-case\">GS<\/jats:styled-content>\u20109669 or <jats:styled-content style=\"fixed-case\">GS<\/jats:styled-content>\u20109451 for 6 weeks (<jats:italic>n<\/jats:italic> = 6, 0 cirrhotics). Nine of ten subjects achieved a sustained virologic response (SVR), while one noncirrhotic subject relapsed. Hepatic IFN\u2010stimulated gene expression decreased with treatment in the liver of all subjects, with no observable impact of cirrhosis. Hepatic gene expression of type <jats:styled-content style=\"fixed-case\">III<\/jats:styled-content> IFNs (<jats:italic><jats:styled-content style=\"fixed-case\">IFNL<\/jats:styled-content>1<\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">IFNL<\/jats:styled-content>3<\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">IFNL<\/jats:styled-content>4\u2010<\/jats:italic>\u0394G) similarly decreased with treatment, while <jats:italic><jats:styled-content style=\"fixed-case\">IFNA<\/jats:styled-content>2<\/jats:italic> expression, undetectable in all subjects pretreatment, was detected post\u2010treatment in three subjects who achieved a SVR. Only the subject who relapsed had detectable <jats:italic><jats:styled-content style=\"fixed-case\">IFNL<\/jats:styled-content>4\u2010<\/jats:italic>\u0394G expression in post\u2010treatment liver. Other IFNs had no change in gene expression (<jats:italic><jats:styled-content style=\"fixed-case\">IFNG<\/jats:styled-content><\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">IFNB<\/jats:styled-content>1<\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">IFNA<\/jats:styled-content>5<\/jats:italic>) or could not be detected. Although expression of multiple hepatic mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s changed with treatment, many mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s previously implicated in <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> replication and IFN signalling had unchanged expression. In conclusion, favourable treatment outcome during IFN\u2010free <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> therapy is associated with changes in the host IFN response regardless of cirrhosis.<\/jats:p>","DOI":"10.1111\/jvh.12510","type":"journal-article","created":{"date-parts":[[2016,2,3]],"date-time":"2016-02-03T16:14:01Z","timestamp":1454516041000},"page":"496-505","source":"Crossref","is-referenced-by-count":38,"title":["Achieving sustained virologic response after interferon\u2010free hepatitis C virus treatment correlates with hepatic interferon gene expression changes independent of cirrhosis"],"prefix":"10.1111","volume":"23","author":[{"given":"E. G.","family":"Meissner","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases Department of Microbiology and Immunology Medical University of South Carolina Charleston SC USA"},{"name":"Laboratory of Immunoregulation National Institute of Allergy and Infectious Diseases National Institutes of Health Bethesda MD USA"},{"name":"Critical Care Medicine Department NIH Clinical Center Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Kohli","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation National Institute of Allergy and Infectious Diseases National Institutes of Health Bethesda MD USA"},{"name":"St Joseph's Hospital and Medical Center Department of Hepatology Creighton University School of Medicine Phoenix AZ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Virtaneva","sequence":"additional","affiliation":[{"name":"Genomics Unit Research Technologies Section Rocky Mountain Laboratories NIAID, NIH Hamilton MT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Sturdevant","sequence":"additional","affiliation":[{"name":"Genomics Unit Research Technologies Section Rocky Mountain Laboratories NIAID, NIH Hamilton MT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Martens","sequence":"additional","affiliation":[{"name":"Genomics Unit Research Technologies Section Rocky Mountain Laboratories NIAID, NIH Hamilton MT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. 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