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Outflanking HCV

Nature Immunology volume 15, pages 6–8 (2014)Cite this article

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Studies have linked polymorphisms near the gene encoding interferon-λ3 (IFNL3) to clearance of hepatitis C virus (HCV). One such favorable polymorphism operates by stabilizing IFNL3 mRNA via a decrease in AU-rich element–mediated decay as well as the binding of HCV-induced host microRNAs.

Infection with hepatitis C virus (HCV) is a worldwide concern that can lead to serious liver conditions, such as cirrhosis and hepatocellular carcinoma. Approximately three to four million people each year are infected with HCV, and more than 350,000 people die from HCV-related liver disease; at present, approximately 185 million people are chronically infected with this virus worldwide. Combinational antiviral therapy, such as interferon-α (IFN-α) plus ribavirin, has been the most widely used strategy for treating HCV. Although most patients respond well to that treatment, certain people remain nonresponsive. Several independent genome-wide association studies have reported an association between genetic polymorphisms in the gene encoding IFN-λ3 (IFNL3) and the outcome of natural clearance of HCV or interferon therapy in patients chronically infected with HCV (genotype 1)1,2,3,4. Although single-nucleotide polymorphisms near IFNL3 have been found to be associated with HCV infection and have been used to predict the outcome of traditional therapy with IFN-α, the molecular mechanism underlying this association remains to be discovered. In this issue of Nature Immunology, McFarland et al. identify a favorable single-nucleotide polymorphism (rs4803217) located in the 3′ untranslated region (UTR) of IFNL3 mRNA that diminishes not only its AU-rich element–mediated decay but also the binding of HCV-induced microRNAs (miRNAs) during infection5.

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Figure 1: The role of HCV-induced miRNAs in HCV clearance.

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  1. Zhigang Tian is with the Institute of Immunology, School of Life Sciences, University of Science and Technology of China, Hefei, China.,

    Zhigang Tian

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Correspondence to Zhigang Tian.

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Tian, Z. Outflanking HCV. Nat Immunol 15, 6–8 (2014). https://doi.org/10.1038/ni.2783

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