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Viral Recombination

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Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.

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Celastrol Inhibits Porcine Epidemic Diarrhea Virus Replication by Promoting ROS-Mediated Apoptosis.

Junhai Zhu¹, Kaifang Yang¹, Pengfei Zhang¹

¹College of Veterinary Medicine, Southwest University, No 2, Tiansheng Street, Chong Qing, 400715, China, swu.edu.cn.

Transboundary and Emerging Diseases

|December 15, 2025

Summary

This summary is machine-generated.

Celastrol effectively inhibits porcine epidemic diarrhea virus (PEDV) replication by inducing apoptosis through a reactive oxygen species (ROS)-dependent mechanism. This natural compound shows promise for controlling swine viral diseases.

Keywords:

antiviral drug apoptosis celastrol network pharmacology porcine epidemic diarrhea virus

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Area of Science:

Veterinary Virology
Natural Product Chemistry
Molecular Virology

Background:

Porcine epidemic diarrhea virus (PEDV) causes significant economic losses in swine production due to high piglet mortality.
Current therapeutic options for PEDV are limited, necessitating the development of novel antiviral strategies.

Purpose of the Study:

To investigate the antiviral activity of celastrol, a natural triterpenoid, against PEDV.
To elucidate the mechanism of action of celastrol in inhibiting PEDV replication.

Main Methods:

In vitro antiviral assays using Vero E6 cells infected with PEDV.
Network pharmacology analysis to identify key signaling pathways.
Mechanistic studies involving reactive oxygen species (ROS) detection and manipulation.

Main Results:

Celastrol significantly inhibited PEDV replication in a dose-dependent manner, targeting postentry viral stages.
Celastrol promoted PEDV-induced ROS accumulation, triggering apoptosis and suppressing viral replication.
Inhibition of ROS abolished celastrol's antiviral effect, confirming a ROS-dependent mechanism.
Celastrol also showed in vitro activity against porcine deltacoronavirus (PDCoV) and porcine reproductive and respiratory syndrome virus (PRRSV).

Conclusions:

Celastrol exhibits potent antiviral activity against PEDV through a ROS-dependent induction of apoptosis.
Celastrol is a promising candidate for the development of novel therapeutics for PEDV and potentially other swine viral infections.