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首页> 外文期刊>Nature immunology >The favorable IFNL3 genotype escapes mRNA decay mediated by AU-rich elements and hepatitis C virus-induced microRNAs
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The favorable IFNL3 genotype escapes mRNA decay mediated by AU-rich elements and hepatitis C virus-induced microRNAs

机译：有利的IFNL3基因型摆脱了富含AU的元素和丙型肝炎病毒诱导的microRNA介导的mRNA降解

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摘要

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.
机译：编码干扰素-λ3（IFN-λ3）的IFNL3在丙型肝炎病毒（HCV）领域引起了相当大的关注，因为许多独立的全基因组关联研究已确定IFNL3附近的多态性与HCV清除之间有很强的关联。但是，这种关联的基础机制仍然难以捉摸。在这项研究中，我们报告了在指示转录稳定性的IFNL3 mRNA 3'非翻译区（UTR）中鉴定功能性多态性（rs4803217）。我们发现这种多态性影响了感染过程中IFN-L3 mRNA的富AU元件（ARE）介导的衰变（AMD），以及HCV诱导的microRNA的结合。这些途径共同介导了不利的IFNL3多态性的强烈抑制。我们的数据揭示了HCV减弱抗病毒反应的先前未知的机制，并表明了HCV治疗的新潜在治疗靶标。

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