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

Mohammed Eslam, Ahmed M. Hashem, Reynold Leung, Manuel Romero-Gomez, Thomas Berg, Gregory J. Dore, Henry L K 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 PowellJacob Nattermann, Stephen Riordan, Duncan McLeod, Nicola J. Armstrong, Mark W. Douglas, Christopher Liddle, David R. Booth, Jacob George, Golo Ahlenstiel, Javier Ampuero, Margaret Bassendine, Vincent W S Wong, Chiara Rosso, Rose White, Lavinia Mezzabotta, Vijayaprakash Suppiah, Monika Michalk, Barbara Malik, Gail Matthews, Tanya Applegate, Jason Grebely, Vincenzo Fragomeli, Julie R. Jonsson, Rosanna Santaro

Research output: Contribution to journalArticlepeer-review


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
JournalNature Communications
Publication statusPublished - 2015

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Chemistry(all)
  • Physics and Astronomy(all)


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