Scholarlink

<p>Long non-coding RNAs (lncRNAs) regulate antiviral immunity against influenza A viruses, yet their roles in natural reservoir hosts like ducks remain unclear. In ducks, Retinoic acid-inducible gene I (RIG-I) contributes to their resistance to infection. To identify duck lncRNAs involved in RIG-I-mediated antiviral responses, we analyzed transcriptomic data from highly pathogenic avian influenza (HPAI)-infected duck lung tissues and identified lnc455 co-expressed with IFNβ. In-silico predictions suggested lnc455 could interact with RIG-I and MAVS, two key signaling proteins in the Type I IFN pathway. Functional assays in chicken cells showed that lnc455 enhances IFNβ promoter activity when co-expressed with either RIG-I or MAVS, even in the absence of viral ligand. However, our data did not show direct binding between lnc455 and RIG-I or MAVS. Instead, lnc455 was associated with Type I IFN negative regulators, including Pur-α, Pur-β, YB-1, HNRNPDL, and HNRNPAB. Notably, overexpression of HNRNPAB reduced MAVS-induced IFNβ activity and MAVS protein abundance, effects that were significantly rescued by lnc455. These findings suggest that lnc455 enhances Type I IFN signaling indirectly by modulating MAVS-associated repression rather than through direct interaction with upstream sensors. Together, our results identify lnc455 as a duck-specific lncRNA that fine-tunes antiviral Type I IFN responses through indirect regulation of the RIG-I/MAVS signaling pathway.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Duck lncRNA lnc455 enhances RIG-I/MAVS type I interferon signaling by modulating hnRNPAB-mediated regulation of MAVS signaling

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月10日

查看全文
  • Renald James Legaspi,
  • Katharine E. Magor

摘要

Long non-coding RNAs (lncRNAs) regulate antiviral immunity against influenza A viruses, yet their roles in natural reservoir hosts like ducks remain unclear. In ducks, Retinoic acid-inducible gene I (RIG-I) contributes to their resistance to infection. To identify duck lncRNAs involved in RIG-I-mediated antiviral responses, we analyzed transcriptomic data from highly pathogenic avian influenza (HPAI)-infected duck lung tissues and identified lnc455 co-expressed with IFNβ. In-silico predictions suggested lnc455 could interact with RIG-I and MAVS, two key signaling proteins in the Type I IFN pathway. Functional assays in chicken cells showed that lnc455 enhances IFNβ promoter activity when co-expressed with either RIG-I or MAVS, even in the absence of viral ligand. However, our data did not show direct binding between lnc455 and RIG-I or MAVS. Instead, lnc455 was associated with Type I IFN negative regulators, including Pur-α, Pur-β, YB-1, HNRNPDL, and HNRNPAB. Notably, overexpression of HNRNPAB reduced MAVS-induced IFNβ activity and MAVS protein abundance, effects that were significantly rescued by lnc455. These findings suggest that lnc455 enhances Type I IFN signaling indirectly by modulating MAVS-associated repression rather than through direct interaction with upstream sensors. Together, our results identify lnc455 as a duck-specific lncRNA that fine-tunes antiviral Type I IFN responses through indirect regulation of the RIG-I/MAVS signaling pathway.