Authors
Mohammed Eslam, Ahmed M Hashem, Reynold Leung, Manuel Romero-Gomez, Thomas Berg, Gregory J Dore, Henry LK Chan, William L Irving, David Sheridan, Maria L Abate, Leon A Adams, Alessandra Mangia, Martin Weltman, Elisabetta Bugianesi, Ulrich Spengler, Olfat Shaker, Janett Fischer, Lindsay Mollison, Wendy Cheng, Elizabeth Powell, Jacob Nattermann, Stephen Riordan, Duncan McLeod, Nicola J Armstrong, Mark W Douglas, Christopher Liddle, David R Booth, Jacob George, Golo Ahlenstiel
Publication date
2015/3/5
Journal
Nature communications
Volume
6
Issue
1
Pages
6422
Publisher
Nature Publishing Group UK
Description
Tissue fibrosis is a core pathologic process that contributes to mortality in ~45% of the population and is likely to be influenced by the host genetic architecture. Here we demonstrate, using liver disease as a model, that a single-nucleotide polymorphism (rs12979860) in the intronic region of interferon-λ4 (IFNL4) is a strong predictor of fibrosis in an aetiology-independent manner. In a cohort of 4,172 patients, including 3,129 with chronic hepatitis C (CHC), 555 with chronic hepatitis B (CHB) and 488 with non-alcoholic fatty liver disease (NAFLD), those with rs12979860CC have greater hepatic inflammation and fibrosis. In CHC, those with rs12979860CC also have greater stage-constant and stage-specific fibrosis progression rates (P<0.0001 for all). The impact of rs12979860 genotypes on fibrosis is maximal in young females, especially those with HCV genotype 3. These findings establish rs12979860 genotype as …
Scholar articles
M Eslam, AM Hashem, R Leung, M Romero-Gomez… - Nature communications, 2015