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Quercetin Regulates Autophagy to Inhibit PRRSV Replication Through the PI3K/Akt/mTOR Signaling Pathway.

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Viruses
|December 31, 2025
PubMed
Summary

Quercetin inhibits Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) replication by modulating autophagy. This natural compound regulates autophagosome degradation and formation via the PI3K/Akt/mTOR pathway, reducing viral load.

Keywords:
PRRSVautophagyquercetin

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Area of Science:

  • Veterinary Virology
  • Molecular Biology
  • Immunology

Background:

  • Porcine Reproductive and Respiratory Syndrome (PRRS) causes substantial economic losses in the swine industry.
  • Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) is a highly contagious pathogen.
  • Autophagy plays a role in viral replication, including PRRSV.

Purpose of the Study:

  • To investigate the antiviral effects of quercetin against PRRSV.
  • To elucidate the mechanism by which quercetin inhibits PRRSV replication, focusing on autophagy modulation.
  • To determine the involvement of the PI3K/Akt/mTOR pathway in quercetin's antiviral activity.

Main Methods:

  • Utilized MARC-45 cells for in vitro PRRSV infection models.
  • Assessed PRRSV replication levels after quercetin treatment.
  • Analyzed autophagy markers, including autophagosome generation and degradation.
  • Investigated the impact of quercetin on the PI3K/Akt/mTOR signaling pathway.

Main Results:

  • Quercetin significantly inhibited PRRSV replication in MARC-45 cells.
  • Quercetin regulated autophagosome degradation and suppressed autophagosome generation.
  • Quercetin suppressed PRRSV-induced autophagy by affecting the PI3K/Akt/mTOR pathway.
  • Quercetin promoted autophagosome-lysosome fusion, leading to reduced viral replication.

Conclusions:

  • Quercetin exhibits antiviral properties against PRRSV by modulating cellular autophagy.
  • The PI3K/Akt/mTOR signaling pathway is a key mediator of quercetin's inhibitory effect on PRRSV replication.
  • Quercetin represents a potential therapeutic agent for PRRSV infections by targeting autophagy mechanisms.