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<p>Influenza virus infection can lead to high mortality and severe disease complicated by secondary bacterial pneumonia. FeiyanHeji (FyHj) is a traditional Chinese medicine (TCM) mixture used clinically to treat pneumonia caused by influenza, although its mechanism of action remains unclear. We first conducted a network pharmacology analysis of the ten components in FyHj to predict their potential interactions with influenza-related targets. GO and KEGG analyses revealed significant enrichment in the inflammatory response, ubiquitin protein binding, RNA virus-related pathways, and the RIG-I signaling pathway, suggesting these may be involved in the anti-influenza process. Further experimental validation demonstrated that FyHj inhibits viral replication through two mechanisms: (1) promoting the degradation of polymerase acidic (PA) protein by interfering with UBP11-mediated K48-linked deubiquitination, and (2) enhancing antiviral innate immunity by upregulating the RIG-I/MAVS signaling pathway and stabilizing MAVS through inhibition of TRIM25-mediated K48-linked ubiquitination of MAVS. Finally, FyHj was observed to reduce lung viral load and inflammation in mice infected with influenza A virus (IAV). In conclusion, FyHj decoction elicits potent antiviral effects through multiple mechanisms, providing a mechanistic basis for the clinical application of FyHj and highlighting its potential as a source for multi-target anti-influenza therapies.</p>

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FeiyanHeji multifunctionally inhibits influenza virus via PA protein degradation and RIG-I signaling pathway potentiation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月22日

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  • Tongtong Cao,
  • Wenqiang Sun,
  • Yan Hu,
  • Chang Liu,
  • Yue Hou,
  • Jing Shu,
  • Ningning Zhang,
  • Qiang He,
  • Wenxian Yang

摘要

Influenza virus infection can lead to high mortality and severe disease complicated by secondary bacterial pneumonia. FeiyanHeji (FyHj) is a traditional Chinese medicine (TCM) mixture used clinically to treat pneumonia caused by influenza, although its mechanism of action remains unclear. We first conducted a network pharmacology analysis of the ten components in FyHj to predict their potential interactions with influenza-related targets. GO and KEGG analyses revealed significant enrichment in the inflammatory response, ubiquitin protein binding, RNA virus-related pathways, and the RIG-I signaling pathway, suggesting these may be involved in the anti-influenza process. Further experimental validation demonstrated that FyHj inhibits viral replication through two mechanisms: (1) promoting the degradation of polymerase acidic (PA) protein by interfering with UBP11-mediated K48-linked deubiquitination, and (2) enhancing antiviral innate immunity by upregulating the RIG-I/MAVS signaling pathway and stabilizing MAVS through inhibition of TRIM25-mediated K48-linked ubiquitination of MAVS. Finally, FyHj was observed to reduce lung viral load and inflammation in mice infected with influenza A virus (IAV). In conclusion, FyHj decoction elicits potent antiviral effects through multiple mechanisms, providing a mechanistic basis for the clinical application of FyHj and highlighting its potential as a source for multi-target anti-influenza therapies.