Journal article

IL28B, HLA-C, and KIR Variants Additively Predict Response to Therapy in Chronic Hepatitis C Virus Infection in a European Cohort: A Cross-Sectional Study

Vijayaprakash Suppiah, Silvana Gaudieri, Nicola J Armstrong, Kate S O'Connor, Thomas Berg, Martin Weltman, Maria Lorena Abate, Ulrich Spengler, Margaret Bassendine, Gregory J Dore, William L Irving, Elizabeth Powell, Margaret Hellard, Stephen Riordan, Gail Matthews, David Sheridan, Jacob Nattermann, Antonina Smedile, Tobias Mueller, Emma Hammond Show all

PLOS MEDICINE | PUBLIC LIBRARY SCIENCE | Published : 2011

Abstract

BACKGROUND: To date, drug response genes have not proved as useful in clinical practice as was anticipated at the start of the genomic era. An exception is in the treatment of chronic hepatitis C virus (HCV) genotype 1 infection with pegylated interferon-alpha and ribavirin (PegIFN/R). Viral clearance is achieved in 40%-50% of patients. Interleukin 28B (IL28B) genotype predicts treatment-induced and spontaneous clearance. To improve the predictive value of this genotype, we studied the combined effect of variants of IL28B with human leukocyte antigen C (HLA-C), and its ligands the killer immunoglobulin-like receptors (KIR), which have previously been implicated in HCV viral control. METHODS ..

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University of Melbourne Researchers

Grants

Awarded by Australian Research Council


Awarded by German Ministry of Education and Research (BMBF)


Awarded by EU


Awarded by BMBF


Awarded by Medical Research Council UK


Awarded by BMBF (German Ministry for Science and Education)


Awarded by H.W. and J. Hector Foundation


Awarded by Medical Research Council


Awarded by National Institute for Health Research


Funding Acknowledgements

VS, DB, GS, and JG were supported by Australian Research Council Roche Linkage Project grant LPO0990067 and the Robert W. Storr Bequest to the Sydney Clinical School, University of Sydney. GD is supported by an Australian National Health and Medical Research Council Practitioner Fellowship. TB is supported by the German Competence Network for Viral Hepatitis (Hep-Net), funded by the German Ministry of Education and Research (BMBF, Grant No. 01 KI 0437, Genetic host factors in viral hepatitis and Genetic Epidemiology Group in viral hepatitis) and by the EU-Vigilance network of excellence combating viral resistance (VIRGIL, Projekt No. LSHM-CT-2004-503359) as well as by the BMBF Project: Host and viral determinants for susceptibility and resistance to hepatitis C virus infection (Grant No. 01KI0787, Project B). DS and MB (Newcastle University, UK) are funded by a Medical Research Council UK project grant G0502028. JN was supported by BMBF (German Ministry for Science and Education) [grant no. 01KI0791] and H.W. and J. Hector Foundation [grant no. M42]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.