Document Type : Original Articles
Authors
1
nigeb
2
Faculty of Veterinary Medicine, Ka.C., Islamic Azad University, Karaj, Iran.
3
Department of Quality Control, Razi Vaccine and Serum Research Institute, Agricultural Research, Education, and Extension Organization (AREEO), Karaj, Iran
4
Department of Animal Biotechnology, Faculty of Agriculture Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), P.O. Box. 14965/161, Tehran, Iran.
5
Department of Clinical Sciences, Faculty of Veterinary Medicine, Ka.C., Islamic Azad University, Karaj, Iran
10.22092/ari.2026.371862.4006
Abstract
Introduction: Foot-and-mouth disease virus (FMDV) is a major viral pathogen of herds. The evidence shows that FMDV disrupts host-cell homeostasis by inducing oxidative stress and apoptosis that may contribute to genomic instability. However, FMDV-associated DNA damage at the cellular level remains insufficiently characterized.
Objective: This study aimed to evaluate the cytotoxic, oxidative, apoptotic, and genotoxic effects of FMDV serotypes A and O in IBRS-2 cells in vitro.
Materials and Methods: The IBRS-2 were contaminated with FMDV serotype A or O at a concentration of 10³ TCID₅₀ mL⁻¹ and compared with the control. Apoptosis was assessed using flow cytometry. Intracellular reactive oxygen species (ROS) generation was measured using the DCFH-DA fluorescence assay. Genomic instability was evaluated by alkaline single-cell gel electrophoresis (SCGE). Statistical analysis was achieved using one-way ANOVA followed by Tukey’s post hoc test, with significance set at p ≤ 0.05.
Results: Infection with both FMDV serotypes significantly augmented apoptosis, ROS production, and DNA damage compared with the control (p ≤ 0.05). Serotype O showed a more cytopathic effect than serotype A, ROS signals, and TM, OTM, and DI values. TM and OTM increased from 16.00 ± 2.13 and 9.00 ± 1.01 in the control to 55.00 ± 6.19 and 27.00 ± 2.46 in the serotype A and to 66.00 ± 6.84 and 34.00 ± 4.03 in the serotype O groups.
Conclusion: These findings highlight genomic instability as a component of FMDV cellular pathogenesis and provide a reason for future studies of virus–host interactions.
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