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<p>Echovirus 30 (E30) is a positive-sense RNA virus in the <i>Picornaviridae</i> family, specifically within the <i>Enterovirus genu.</i> It is a known pathogen that causes severe infectious diseases in humans. However, mechanisms underlying viral infection remain poorly understood. Therefore, this study aims to elucidate the mechanisms underlying E30 infection. A whole-genome CRISPR/Cas9 gene knockout screen was employed, and it was observed that knocking out ADP-ribosylation factor GTPase activating protein 1 (ARFGAP1) significantly reduced E30 replication. Subsequent analysis revealed that ARFGAP1 influencing the early stages and internalization of viral infection. Transcriptomic analysis further demonstrated that ARFGAP1 plays a crucial role in vesicular transport. Animal infection studies demonstrated that QS11-mediated inhibition of ARFGAP1 significantly decreased viral replication in mice with homozygous gene knock-out of both the human neonatal Fc receptor and the interferon-alpha/beta receptor (hFcRn-IFNAR<sup><i>−/−</i></sup> mice), mitigated tissue damage, and enhanced survival rates. This study identifies ARFGAP1 as a crucial host factor that promotes E30 infection, offering in depth understanding of the viral infection mechanisms and potential antiviral therapies.</p>

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ARFGAP1 serves as a critical host factor during E30 infection: QS11 inhibits viral pathogenesis in hFcRn-IFNAR−/− mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月29日

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  • Jichen Li,
  • Wei Duan,
  • Ying Liu,
  • Rui Wang,
  • Qian Yang,
  • Huijie Li,
  • Yucai Liang,
  • Jinbo Xiao,
  • Jianfang Zhou,
  • Qiang Sun,
  • Yong Zhang

摘要

Echovirus 30 (E30) is a positive-sense RNA virus in the Picornaviridae family, specifically within the Enterovirus genu. It is a known pathogen that causes severe infectious diseases in humans. However, mechanisms underlying viral infection remain poorly understood. Therefore, this study aims to elucidate the mechanisms underlying E30 infection. A whole-genome CRISPR/Cas9 gene knockout screen was employed, and it was observed that knocking out ADP-ribosylation factor GTPase activating protein 1 (ARFGAP1) significantly reduced E30 replication. Subsequent analysis revealed that ARFGAP1 influencing the early stages and internalization of viral infection. Transcriptomic analysis further demonstrated that ARFGAP1 plays a crucial role in vesicular transport. Animal infection studies demonstrated that QS11-mediated inhibition of ARFGAP1 significantly decreased viral replication in mice with homozygous gene knock-out of both the human neonatal Fc receptor and the interferon-alpha/beta receptor (hFcRn-IFNAR−/− mice), mitigated tissue damage, and enhanced survival rates. This study identifies ARFGAP1 as a crucial host factor that promotes E30 infection, offering in depth understanding of the viral infection mechanisms and potential antiviral therapies.