ArticleVeterinary research2023
Porcine epidemic diarrhea virus activates PERK-ROS axis to benefit its replication in Vero E6 cells.
Article in Veterinary research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Biochanin A Exerts Broad-Spectrum Antiviral Activity Against Coronaviruses via Activating the AMPK/Nrf2/GSH Pathway.Microorganisms · 2026Article
- Porcine epidemic diarrhea virus promotes viral replication via ROS/HIF-1α-mediated glycolysis.Redox biology · 2026Article
- Celastrol Inhibits Porcine Epidemic Diarrhea Virus Replication by Promoting ROS-Mediated Apoptosis.Transboundary and emerging diseases · 2025Article
- Small GTP-binding protein GDP dissociation stimulator influences cisplatin-induced acute kidney injury via PERK-dependent ER stress.Communications biology · 2024Article
- Endoplasmic reticulum stress in diseases.MedComm · 2024Review
- Regulatory effects of Trichinella spiralis serpin-type serine protease inhibitor on endoplasmic reticulum stress and oxidative stress in host intestinal epithelial cells.Veterinary research · 2024Article
- Insights into the Activation of Unfolded Protein Response Mechanism during Coronavirus Infection.Current issues in molecular biology · 2024Review
- Towards a Safer Future: Enhancing Vaccine Development to Combat Animal Coronaviruses.Vaccines · 2024Review
- Human Betacoronavirus OC43 Interferes with the Integrated Stress Response Pathway in Infected Cells.Viruses · 2024Article
- DHA and EPA inhibit porcine coronavirus replication by alleviating ER stress.Journal of virology · 2023Article
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Of the three branches of unfolded protein response (UPR) that were reportedly activated by porcine epidemic diarrhea virus (PEDV), PERK is recently shown to act as an upstream regulator of oxidative response of the cells. However, it remains unknown if and how PERK activation during PEDV infection would result in oxidative stress, and whether activation of PERK and its downstream molecules affect PEDV replication. Here, we demonstrate that infection with the PEDV strain YJH/2015 triggered UPR in Vero E6 cells by activating the PERK/eIF2α pathway and led to significant increase in the expression of proapoptotic protein C/EBP homologous protein (CHOP) and ER oxidoreductase 1 alpha (ERO1α). Inhibition of PERK by short hairpin RNA (shRNA) or GSK2606414 and knockdown of CHOP by small interfering RNA reduced expression of ERO1α and generation of ROS in PEDV-infected cells. Inhibition of ERO1α by shRNA or EN460 decreased PEDV-induced ROS generation. Genetic or pharmacological inhibition of each component of PERK, CHOP, ERO1α, and ROS led to significant suppression of PEDV replication. Collectively, our study provides the first evidence that PEDV manipulates endoplasmic reticulum to perturb its redox homeostasis via the PERK-CHOP-ERO1α-ROS axis in favor of its replication.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.