ArticleVirology journal2025
ARFGAP1 serves as a critical host factor during E30 infection: QS11 inhibits viral pathogenesis in hFcRn-IFNAR
Article in Virology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
11 authors.
Funding
Abstract
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
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