Association of IFNL3 rs12979860 and rs8099917 with biochemical predictors of interferon responsiveness in chronic hepatitis C virus infection

PLoS One. 2013 Oct 29;8(10):e77530. doi: 10.1371/journal.pone.0077530. eCollection 2013.

Abstract

Background & aims: Genetic variations near the interferon lambda 3 gene (IFNL3, IL28B) are the most powerful predictors for sustained virologic response (SVR) in patients with chronic hepatitis C virus (HCV) infection, compared to other biochemical or histological baseline parameters. We evaluated whether the interplay of both IFNL3 polymorphisms rs12979860 and rs8099917 together with non-genetic clinical factors contributes to the predictive role of these genetic variants.

Methods: The cohort comprised 1,402 patients of European descent with chronic HCV type 1 infection. 1,298 patients received interferon-based antiviral therapy, and 719 (55%) achieved SVR. The IFNL3 polymorphisms were genotyped by polymerase chain reaction and melting curve analysis.

Results: A significant correlation was found between the IFNL3 polymorphisms and biochemical as well as virologic predictors of treatment outcome such as ALT, GGT, cholesterol, and HCV RNA levels. In multivariate regression analysis, IFLN3 SNPs, HCV RNA levels, and the GGT/ALT ratio were independent predictors of SVR. Dependent on the GGT/ALT ratio and on the HCV RNA concentration, significant variations in the likelihood for achieving SVR were observed in both, carriers of the responder as well as non-responder alleles.

Conclusions: Our data support a clear association between IFNL3 genotypes and baseline parameters known to impact interferon responsiveness. Improved treatment outcome prediction was achieved when these predictors were considered in combination with the IFNL3 genotype.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antiviral Agents / therapeutic use*
  • Female
  • Genotype
  • Hepacivirus / drug effects
  • Hepatitis C, Chronic / drug therapy*
  • Hepatitis C, Chronic / genetics*
  • Humans
  • Interferons / therapeutic use*
  • Interleukins / genetics*
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide / genetics*
  • Treatment Outcome
  • White People / genetics

Substances

  • Antiviral Agents
  • interferon-lambda, human
  • Interleukins
  • Interferons

Grants and funding

This work was supported by the German Competence Network for Viral Hepatitis (Hep-Net), funded by the German Ministry of Education and Research (BMBF, grant number 01 KI 0437, project number 10.1.3 and Core Project number 10.1, grant number 01KI0787), by the EU-Vigilance network of excellence combating viral resistance (VIRGIL, project number LSHM-CT-2004-503359). Parts of the work were supported by an Australian Research Council Linkage Project Grant (LPO0990067), a National Health and Medical Research Council Grant (1006759) and the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.