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<p>Pteropine orthoreovirus (PRV) is a fusogenic virus carried by bats that causes respiratory illnesses in humans. Micafungin (MCFG), an approved drug for treatment of fungal infections, has been shown to inhibit the propagation of PRV, but its precise mechanism of action remains unclear. In this study, we investigated the molecular mechanism of action of MCFG against PRV propagation. A molecular docking simulation showed that the p17 protein of PRV is likely to be the primary target of MCFG. Differential gene expression analysis was performed to compare MCFG-treated PRV-infected host cells with untreated infected cells, and IL-6 was found to be the main regulator induced by MCFG. Silencing of IL-6 using siRNA resulted in markedly increased levels of PRV release and syncytium formation and marginally increased PRV RNA replication. Treatment with an antibody against p17, the presumed target of MCFG, markedly reduced syncytium formation but did not influence viral RNA replication. In contrast, MCFG significantly suppressed syncytium formation and slightly reduced PRV RNA replication, and MCFG and anti-p17 antibody both increased IL-6 mRNA expression. Molecular docking analysis also suggested that MCFG might inhibit other PRV proteins, including the nonstructural replication protein σNS. In conclusion, it is likely that MCFG primarily targets p17 and modulates host immunity through IL-6, which probably interferes directly with syncytium formation.</p>

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The mechanism of action of micafungin against pteropine orthoreovirus infection in the human A549 cell line

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月25日

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  • Wirayatida Bubphasook,
  • Atsuo Iida,
  • Eiichi Hondo

摘要

Pteropine orthoreovirus (PRV) is a fusogenic virus carried by bats that causes respiratory illnesses in humans. Micafungin (MCFG), an approved drug for treatment of fungal infections, has been shown to inhibit the propagation of PRV, but its precise mechanism of action remains unclear. In this study, we investigated the molecular mechanism of action of MCFG against PRV propagation. A molecular docking simulation showed that the p17 protein of PRV is likely to be the primary target of MCFG. Differential gene expression analysis was performed to compare MCFG-treated PRV-infected host cells with untreated infected cells, and IL-6 was found to be the main regulator induced by MCFG. Silencing of IL-6 using siRNA resulted in markedly increased levels of PRV release and syncytium formation and marginally increased PRV RNA replication. Treatment with an antibody against p17, the presumed target of MCFG, markedly reduced syncytium formation but did not influence viral RNA replication. In contrast, MCFG significantly suppressed syncytium formation and slightly reduced PRV RNA replication, and MCFG and anti-p17 antibody both increased IL-6 mRNA expression. Molecular docking analysis also suggested that MCFG might inhibit other PRV proteins, including the nonstructural replication protein σNS. In conclusion, it is likely that MCFG primarily targets p17 and modulates host immunity through IL-6, which probably interferes directly with syncytium formation.