AI Article Synopsis
- Research highlights the importance of the IFNL3 gene and its link to hepatitis C virus (HCV) clearance through polymorphisms.
- A specific functional polymorphism (rs4803217) in the 3' UTR of IFNL3 mRNA affects its stability and influences decay processes.
- The study uncovers a new mechanism by which HCV can dampen the body's antiviral response, suggesting new potential targets for HCV therapies.
Article Abstract
IFNL3, which encodes interferon-λ3 (IFN-λ3), has received considerable attention in the hepatitis C virus (HCV) field, as many independent genome-wide association studies have identified a strong association between polymorphisms near IFNL3 and clearance of HCV. However, the mechanism underlying this association has remained elusive. In this study, we report the identification of a functional polymorphism (rs4803217) in the 3' untranslated region (UTR) of IFNL3 mRNA that dictated transcript stability. We found that this polymorphism influenced AU-rich element (ARE)-mediated decay (AMD) of IFNL3 mRNA, as well as the binding of HCV-induced microRNAs during infection. Together these pathways mediated robust repression of the unfavorable IFNL3 polymorphism. Our data reveal a previously unknown mechanism by which HCV attenuates the antiviral response and indicate new potential therapeutic targets for HCV treatment.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4183367 | PMC |
| http://dx.doi.org/10.1038/ni.2758 | DOI Listing |
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