Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance

Dongliang Ge, Jacques Fellay, Alexander J. Thompson, Jason S. Simon, Kevin V. Shianna, Thomas J. Urban, Erin L. Heinzen, Ping Qiu, Arthur H. Bertelsen, Andrew J. Muir, Mark Sulkowski, John G. McHutchison and David B. Goldstein ()
Additional contact information
Dongliang Ge: Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA
Jacques Fellay: Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA
Alexander J. Thompson: School of Medicine, Duke University, Durham, North Carolina 27705, USA
Jason S. Simon: Schering-Plough Research Institute, Kenilworth, New Jersey 07033, USA
Kevin V. Shianna: Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA
Thomas J. Urban: Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA
Erin L. Heinzen: Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA
Ping Qiu: Schering-Plough Research Institute, Kenilworth, New Jersey 07033, USA
Arthur H. Bertelsen: Schering-Plough Research Institute, Kenilworth, New Jersey 07033, USA
Andrew J. Muir: School of Medicine, Duke University, Durham, North Carolina 27705, USA
Mark Sulkowski: Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
John G. McHutchison: School of Medicine, Duke University, Durham, North Carolina 27705, USA
David B. Goldstein: Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA

Nature, 2009, vol. 461, issue 7262, 399-401

Abstract: Individual responses to hepatitis C virus Hepatitis C is one of the most common infections in the world. Many of its estimated 170 million sufferers live with the disease for years with no serious symptoms, but in about one in four patients it leads to cirrhosis of the liver. The discovery of a biomarker that predicts an individual's response to hepatitis C treatment raises the possibility that clinical outcomes could be improved by raising patient compliance to the often demanding interferon treatment regime. The new marker is a 'single letter' genetic variant — a C (cytosine) replacing a T (thymidine) in a segment of DNA near the IL28B gene that encodes interleukin 28B (interferon-γ-3). This finding goes some way towards explaining the different treatment outcomes between individuals of European (high IL28B frequency), African and Asian ancestry. And importantly, it is of immediate clinical utility.

Date: 2009
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DOI: 10.1038/nature08309

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