Vitamin E Restricts Senecavirus A Replication in Cell and Mouse Models

Treatment with a form of vitamin E suppresses the replication of Senecavirus A and mitigates ferroptosis-associated oxidative injury in cell culture and animal models, according to a study published in BMC Veterinary Research.

Senecavirus A is a viral pathogen that causes vesicular disease in pigs, prompting research into therapeutic strategies capable of limiting viral multiplication alongside infection-induced host damage. To assess potential protective mechanisms, the research team evaluated purified d-alpha-tocopherol, a form of vitamin E, across cultured porcine PK-15 cells and a mouse model of infection.

In the PK-15 cell experiments, vitamin E reduced both viral RNA abundance and the yield of infectious viral particles. The strongest antiviral effect occurred at a concentration of 20 micromolar, where abundance of the viral VP1 RNA decreased by approximately 87 percent and infectious viral titers exhibited a 1.34-log10 reduction.

The observed viral suppression in porcine cells coincided with biochemical evidence of reduced oxidative stress and preserved antioxidant defenses. The treatment elevated intracellular glutathione content, increased the expression of glutathione peroxidase 4, and lowered indicators of cellular oxidative injury, while the ferroptosis inhibitor ferrostatin-1 also suppressed viral replication alongside characteristic ferroptosis-related changes.

Additional experiments combining virological and redox measurements examined how host antioxidant status influences viral control. Supplementation with glutathione independently reduced infectious virus production, whereas experimental depletion of glutathione partially diminished the antiviral activity of vitamin E, confirming that cellular glutathione availability contributes to the inhibitory response.

In vivo trials in mice demonstrated that administering 20 milligrams per kilogram of vitamin E twelve hours after infection reduced relative viral RNA levels across all five examined tissues. Furthermore, hematoxylin and eosin staining of liver tissue from treated animals showed a hepatocyte arrangement resembling uninfected control tissue, leading the authors to support further evaluation of vitamin E as a candidate host-directed antiviral against Senecavirus A.

Subject of Research: Antiviral activity of vitamin E against Senecavirus A

Article Title: Vitamin E restricts Senecavirus A replication and attenuates ferroptosis-associated oxidative injury

Article References: Huang, J., Zhou, H., Ran, X., Yang, X., & Wen, X. (2026). Vitamin E restricts Senecavirus A replication and attenuates ferroptosis-associated oxidative injury. BMC Veterinary Research. https://doi.org/10.1186/s12917-026-06110-6

Image Credits: AI Generated

DOI: 10.1186/s12917-026-06110-6

Keywords: Senecavirus A, vitamin E, d-alpha-tocopherol, ferroptosis, oxidative injury, PK-15 cells, glutathione, glutathione peroxidase 4, GPX4, ferrostatin-1, VP1 RNA, viral replication, vesicular disease, swine viruses, mouse models, hepatocytes, host-directed antivirals