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. 2023 Feb 3;54:9. doi: 10.1186/s13567-023-01139-z

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Schematic illustration of PEDV-induced activation of the PERK-CHOP-ERO1α axis and increased generation of ROS to promote viral replication in Vero E6 cells. PEDV infection induces ER stress by activating the PERK-eIF2α pathway which in turn activates CHOP. CHOP transcriptionally upregulates ERO1α which initiates oxidative stress by generating ROS during protein folding. Inhibition of PERK by shRNA or GSK2606414, CHOP knockdown by siRNA or ERO1α inhibition by shRNA or EN460 all lead to alleviation of ROS generation and reduced viral replication in PEDV-infected Vero E6 cells.