# The monkeypox virus suppresses autophagy by modulating Rubicon expression

## TL;DR

Monkeypox virus suppresses a cellular process called autophagy by increasing Rubicon levels, which could lead to new treatment strategies.

## Contribution

The study reveals a new mechanism by which monkeypox virus inhibits autophagy through Rubicon modulation.

## Key findings

- Monkeypox virus impairs autophagic flux by upregulating Rubicon.
- Silencing Rubicon restores autophagy and reduces virus replication.
- The findings suggest autophagy activation as a potential therapeutic approach against monkeypox.

## Abstract

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.