ArticleVirulence2025
PRRSV evades innate immune cGAS-STING antiviral function via its Nsp5 to deter STING translocation and activation.
Article in Virulence, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Pathogenicity and virulence of PRRSV: From regulated cell death reprogramming landscape and immune subversion to precision vaccinology.Virulence · 2026Review
- Lectin-Based Antiviral Strategies for Porcine Reproductive and Respiratory Syndrome Virus 2 Infection: Griffithsin Suppresses Viral Replication In Vitro and Reduces Early Viremia In Vivo.Microorganisms · 2026Article
- STING agonists as antiviral agents.FEBS letters · 2026Review
- Duck plague virus LORF2 utilizes RNF34 to inhibit antiviral innate immunity by ubiquitination and degradation of IRF7.PLoS pathogens · 2026Article
- STING Degradation by PRRSV Activates HKViruses · 2026Article
- Sodium Copper Chlorophyllin Inhibits Porcine Reproductive and Respiratory Syndrome Virus Infection Through Multiple Antiviral Mechanisms.Transboundary and emerging diseases · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
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Abstract
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) is an important pathogen that seriously endangers pig breeding, causing significant economic losses to the global swine industry. Our previous study found that the DNA sensing innate cGAS-STING signaling pathway plays an important role in inducing interferon (IFN) upon PRRSV infection and inhibition of PRRSV replication. However, the mechanism underlying immune evasion by PRRSV remains unclear. In the current study, we found that PRRSV non-structural protein 5 (Nsp5) strongly inhibits the cGAS-STING-IFN antiviral response. Furthermore, we found that Nsp5 interacts with STING, blocking STING transport from the ER to the Golgi apparatus and interfering with STING recruitment of TBK1/IKKε/IRF3. Finally, we demonstrated that the Nsp5 36-47 and 58-67 amino acid regions are critical for inhibiting STING activity and PRRSV replication. This study describes a novel mechanism by which PRRSV suppresses the host innate antiviral response and has implications for our understanding of PRRSV pathogenesis.
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