The Role of Interferon-λ Locus Polymorphisms in Hepatitis C and Other Infectious Diseases

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Abstract

Since its discovery in 2003, the type III interferon-λ (IFN-λ) family has been found to contribute significantly to the host response to infection. Whilst IFN-λ shares many features with type I IFN induction and signalling pathways, the tissue-specific restricted expression of its receptor, IL28RA, makes IFN-λ a major mediator of host innate immunity in tissues and organs with a high epithelial cell content. Host susceptibility and responses to infection are known to be heterogeneous, and the identification of common genetic variants linked to disease outcome by genome-wide association studies (GWAS) has underscored the significance of host polymorphisms in responses to infection. Several such GWAS have highlighted the IFN-λ locus on chromosome 19q13 as an area of genetic variation significantly associated with hepatitis C virus (HCV) infection, and the rs12979860 genotype can be used in clinical practice as a biomarker for predicting a successful response to treatment with pegylated IFN and ribavarin. Here, we discuss IFN-λ genetic polymorphisms and their role in HCV and other infectious diseases as well as their potential impact on clinical diagnostics, patient stratification and therapy. Finally, the broader role of IFN-λ in the immunopathogenesis of non-infectious inflammatory diseases is considered. © 2015 S. Karger AG, Basel.

Original languageEnglish
Pages (from-to)231–242
JournalJournal of Innate Immunity
Volume7
Issue number3
Early online date23 Jan 2015
DOIs
Publication statusPublished - Apr 2015

Keywords

  • Interferon-λ
  • Virology
  • Immune response
  • Host defence
  • Epithelium
  • Cytokines
  • Autoimmunity
  • Hepatitis C virus
  • Single-nucleotide polymorphism
  • Polymorphism
  • IL28B

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