Interferon-λ rs12979860 genotype and liver fibrosis in viral and non-viral chronic liver disease

M. Eslam, A.M.A. Hashem, R. Leung, M. Romero-Gómez, T. Berg, G.J. Doré, H.L.K. Chan, W.L. Irving, D.A. Sheridan, M.L. Abate, Leon Adams, A. Mangia, M.D. Weltman, E. Bugianesi, U. Spengler, O.G.A. Shaker, J. Fischer, L.C. Mollison, W. Cheng, E.E. PowellJ. Nattermann, S.M. Riordan, D.J. Mcleod, N.J. Armstrong, M.W.W. Douglas, C. Liddle, D.R. Booth, J. George, G. Ahlenstiel, J.A. Ampuero, M.F. Bassendine, V.W.S. Wong, C. Rosso, R. White, L. Mezzabotta, V. Suppiah, M. Michalk, B. Malik, G.V. Matthews, T.L. Applegate, J. Grebely, V. Fragomeli, J.R. Jonsson, R. Santaro

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    © 2015 Macmillan Publishers Limited. All rights reserved. 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
    Original languageEnglish
    Article number6422
    Number of pages10
    JournalNature Communications
    Publication statusPublished - 5 Mar 2015


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