ArticleBMC microbiology2025
Rosmarinic Acid inhibits Pseudorabies Virus (PRV) infection by activating the cGAS-STING signaling pathway.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The roles and mechanisms of natural compounds in preventing and treating viral reproductive disorders in major economic livestock.Virulence · 2026Review
- Isoliquiritigenin Elicits Potent Antiviral Activity Against Pseudorabies Virus Through Modulating the cGAS/STING and JAK/STAT Signaling Cascades.Veterinary sciences · 2026Article
- Lactobacillus Plantarum R-Fermented Phellodendron Amurense Extract Protects Against Pseudorabies Virus by Regulating Oxidative Stress and Inflammation in Vitro and in Vivo.Probiotics and antimicrobial proteins · 2026Article
- Rosmarinic Acid Inhibits PRV Replication by Regulating Oxidative Stress Through the Nrf2 Signaling Pathway.Animals : an open access journal from MDPI · 2026Article
- Article
- The tegument protein VP22 of pseudorabies virus inhibits cGAS condensation by inducing nuclear-to-cytoplasmic translocation of DDX21.PLoS pathogens · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudorabies virus (PRV), a swine alphaherpesvirus, is a double-stranded DNA virus. It may infect various animals, especially pigs. PRV infection in pigs leads to high mortality rates, and causes huge economic lose for swine industry. Currently, there are few effective antiviral treatments available. Rosmarinic acid (RA), a hydrophilic phenolic compound, shows potential for inhibiting herpes simplex virus. Given that PRV is a member of the Herpesviridae family, this study investigated the antiviral effects of RA against PRV infection through both in vitro and in vivo, as well as the underlying molecular mechanisms. PK-15 cells were used to assess the cytotoxicity of RA in vitro, followed by an investigation of its anti-PRV activity. The study then explored how RA regulates the cGAS-STING signaling pathway, along with inflammatory and apoptotic factors in PRV-infected cells. Molecular docking and dynamics simulations further elucidated the binding interactions between RA and cGAS-STING, providing insight into how RA activates the cGAS-STING pathway against PRV infection. In vivo, the antiviral efficacy of RA was evaluated in a PRV-infected mouse model by assessing tissue viral genome copies, the innate immune cGAS-STING signaling pathway activation, and inflammatory and apoptotic responses. The results showed that RA exhibited a half-maximal cytotoxic concentration (CC
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Registered trials
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