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<p>Monkeypox virus (MPXV) is a globally reemerging pathogen that poses a significant threat to public health, representing the most impactful Orthopoxvirus infection in humans since the eradication of smallpox. Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved catabolic process essential for maintaining cellular homeostasis, and it can exert either pro-viral or anti-viral effects during infections. Poxviruses interaction with the autophagy machinery remains poorly understood, and the specific interplay between MPXV and autophagy has not been documented. In this study, we infected Calu-3 cells with MPXV and observed that the virus significantly impairs autophagic flux by upregulating Rubicon, a known negative regulator of autophagy. Notably, silencing Rubicon restored autophagic flux and led to a marked reduction in MPXV replication. Overall, our findings reveal a novel mechanism by which MPXV inhibits autophagy through the modulation of Rubicon, suggesting that autophagy activation may be a potential therapeutic strategy for MPXV.</p>

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The monkeypox virus suppresses autophagy by modulating Rubicon expression

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月23日

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  • Giulia Refolo,
  • Cosmina Mija,
  • Fabiola Ciccosanti,
  • Giuseppe Sberna,
  • Valentina Mazzotta,
  • Fabrizio Maggi,
  • Mauro Piacentini,
  • Tiziana Vescovo,
  • Licia Bordi

摘要

Monkeypox virus (MPXV) is a globally reemerging pathogen that poses a significant threat to public health, representing the most impactful Orthopoxvirus infection in humans since the eradication of smallpox. Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved catabolic process essential for maintaining cellular homeostasis, and it can exert either pro-viral or anti-viral effects during infections. Poxviruses interaction with the autophagy machinery remains poorly understood, and the specific interplay between MPXV and autophagy has not been documented. In this study, we infected Calu-3 cells with MPXV and observed that the virus significantly impairs autophagic flux by upregulating Rubicon, a known negative regulator of autophagy. Notably, silencing Rubicon restored autophagic flux and led to a marked reduction in MPXV replication. Overall, our findings reveal a novel mechanism by which MPXV inhibits autophagy through the modulation of Rubicon, suggesting that autophagy activation may be a potential therapeutic strategy for MPXV.