Genetic variation at IFNL4 influences extrahepatic interferon-stimulated gene expression in chronic HCV patients Academic Article uri icon

Overview

MeSH Major

  • Hepacivirus
  • Hepatitis C, Chronic
  • Liver Cirrhosis

abstract

  • Polymorphisms at IFNL4 strongly influence spontaneous resolution and interferon therapeutic response in hepatitis C virus (HCV) infection. In chronic HCV, unfavorable alleles are associated with elevated interferon (IFN)-stimulated gene (ISG) expression in the liver, but extrahepatic effects are less well characterized. We used RNA sequencing (RNA-Seq) to examine whether IFNL4 genetic variation (rs368234815) modulates ISG expression in peripheral blood mononuclear cells (PBMC) during chronic HCV infection. ISG expression was elevated in unstimulated PBMC homozygous for the unfavorable ΔG IFNL4 variant; expression following IFN-α stimulation was comparable across genotypes. These findings suggest that lambda interferons may have broader systemic effects during HCV infection.

publication date

  • February 15, 2018

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC5853921

Digital Object Identifier (DOI)

  • 10.1093/infdis/jix593

PubMed ID

  • 29165633

Additional Document Info

start page

  • 650

end page

  • 655

volume

  • 217

number

  • 4