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<p>Enteroviruses, which belong to the Picornaviridae family, include species that infect humans and Interferon Alpha (IFNα) is commonly used against Enterovirus 71 (EV71) infections. This study investigated the role of IFNα-induced miR-362-3p expression in the defense against EV71EV71. Differential analysis identified up-regulated miRNAs following IFNα treatment. RD cells were used to assess EV71proliferation, while HMC3 cells were employed to evaluate the effects of IFNα and EV71 on miR-362-3p expression. Antiviral activity was assessed by modulating miR-362-3p levels. Compared to the NC mimic group, miR-362-3p in miR-362-3p mimic and IFNα treatment groups was increased; cell viability was enhanced; -lgTCID50 was reduced, and the replication of EV71 was inhibited. Further, VP1 mRNA and protein expression declined significantly in miR-362-3p mimic group vs NC mimic while they were notably elevated in the miR-362-3p inhibitor group vs NC inhibitor. IFNα treatment could induce miR-362-3p production and enhanced cell viability in HMC3 cells. Besides, when compared with the miR-362-3p mimic group, IFNα combined with miR-362-3p mimic group reduced -lgTCID50 and significantly decreased the expression of VP1 mRNA and protein. Conclusion: The inhibition of EV71-infected HMC3 cell replication was related to the upregulation of miR-362-3p induced by IFNα, which in turn enhanced antiviral viability.</p>

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MiR-362-3p mediates IFNα-induced antiviral viability against Enterovirus 71 (EV71)

  • 期刊论文

  • 发表日期：

    2025年3月26日

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  • San Wang,
  • Lan Chen,
  • Zongtao Wu,
  • Yingbo Zou,
  • Yunrong Li,
  • Xiang He,
  • Yusong Zhang,
  • Bo Huang

摘要

Enteroviruses, which belong to the Picornaviridae family, include species that infect humans and Interferon Alpha (IFNα) is commonly used against Enterovirus 71 (EV71) infections. This study investigated the role of IFNα-induced miR-362-3p expression in the defense against EV71EV71. Differential analysis identified up-regulated miRNAs following IFNα treatment. RD cells were used to assess EV71proliferation, while HMC3 cells were employed to evaluate the effects of IFNα and EV71 on miR-362-3p expression. Antiviral activity was assessed by modulating miR-362-3p levels. Compared to the NC mimic group, miR-362-3p in miR-362-3p mimic and IFNα treatment groups was increased; cell viability was enhanced; -lgTCID50 was reduced, and the replication of EV71 was inhibited. Further, VP1 mRNA and protein expression declined significantly in miR-362-3p mimic group vs NC mimic while they were notably elevated in the miR-362-3p inhibitor group vs NC inhibitor. IFNα treatment could induce miR-362-3p production and enhanced cell viability in HMC3 cells. Besides, when compared with the miR-362-3p mimic group, IFNα combined with miR-362-3p mimic group reduced -lgTCID50 and significantly decreased the expression of VP1 mRNA and protein. Conclusion: The inhibition of EV71-infected HMC3 cell replication was related to the upregulation of miR-362-3p induced by IFNα, which in turn enhanced antiviral viability.