NDLI: Variants in interferon-alpha pathway genes and response to pegylated interferon-Alpha2a plus ribavirin for treatment of chronic hepatitis C virus infection in the hepatitis C antiviral long-term treatment against cirrhosis trial.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Welzel, Tania Mara Morgan, Timothy R. Bonkovsky, Herbert L. Naishadham, Deepa Pfeiffer, Ruth M. Wright, Elizabeth C. Hutchinson, Amy A. Crenshaw, Andrew T. Bashirova, Arman Carrington, Mary Dotrang, Myhanh Sterling, Richard K. Lindsay, Karen L. Fontana, Robert J. Lee, William M. Di Bisceglie, Adrian M. Ghany, Marc G. Gretch, David R. Chanock, Stephen J. Chung, Raymond T. O'Brien, Thomas R.
Description	Country affiliation: United States Author Affiliation: Welzel TM ( Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA.)
Abstract	UNLABELLED: Combination treatment with pegylated-interferon-alpha (PEG IFN-alpha) and ribavirin, the current recommended therapy for chronic hepatitis C virus (HCV) infection, results in a sustained virological response (SVR) in only about half of patients. Because genes involved in the interferon-alpha pathway may affect antiviral responses, we analyzed the relationship between variants in these genes and SVR among participants in the Hepatitis C Antiviral Long-Term treatment Against Cirrhosis (HALT-C) trial. Patients had advanced chronic hepatitis C that had previously failed to respond to interferon-based treatment. Participants were treated with peginterferon-alpha2a and ribavirin during the trial. Subjects with undetectable HCV RNA at week 72 were considered to have had an SVR. Subjects with detectable HCV RNA at week 20 were considered nonresponders. We used TaqMan assays to genotype 56 polymorphisms found in 13 genes in the interferon-alpha pathway. This analysis compares genotypes for participants with an SVR to nonresponders. The primary analysis was restricted to European American participants because a priori statistical power was low among the small number (n = 131) of African American patients. We used logistic regression to control the effect of other variables that are associated with treatment response. Among 581 European American patients, SVR was associated with IFNAR1 IVS1-22G (adjusted odds ratio, 0.57; P = 0.02); IFNAR2 Ex2-33C (adjusted odds ratio, 2.09; P = 0.02); JAK1 IVS22+112T (adjusted odds ratio, 1.66; P = 0.04); and ADAR Ex9+14A (adjusted odds ratio, 1.67; P = 0.03). For the TYK2-2256A promoter region variant, a borderline association was present among European American participants (OR, 1.51; P = 0.05) and a strong relationship among African American patients; all 10 with SVR who were genotyped for TYK2 -2256 carried the A variant compared with 68 of 120 (57%) nonresponders (P = 0.006). CONCLUSION: Genetic polymorphisms in the interferon-alpha pathway may affect responses to antiviral therapy of chronic hepatitis C.
File Format	HTM / HTML
ISSN	02709139
e-ISSN	15273350
DOI	10.1002/hep.22877
Journal	Hepatology
Issue Number	6
Volume Number	49
Language	English
Publisher	Wiley
Publisher Date	2009-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Hepatology Antiviral Agents Administration & Dosage Hepatitis C, Chronic Drug Therapy Genetics Interferon-alpha Liver Cirrhosis Etiology Polyethylene Glycols Ribavirin Drug Therapy, Combination Complications Polymorphism, Genetic Recombinant Proteins Time Factors Research Support, N.i.h., Extramural Research Support, N.i.h., Intramural
Content Type	Text
Resource Type	Article
Subject	Hepatology

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