ArticleThe Journal of general virology2015
Porcine reproductive and respiratory syndrome virus 3C protease cleaves the mitochondrial antiviral signalling complex to antagonize IFN-β expression.
Article in The Journal of general virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 49 citations in OpenAlex.
- Equine arteritis virus Nsp10 promotes MAVS proteasomal degradation via E3 ligases Smurf1/MARCH5.Journal of virology · 2026Article
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- Advances in the immunosuppression of porcine reproductive and respiratory syndrome virus.Frontiers in veterinary science · 2026Review
- Identification of two conserved B-cell epitopes targeting NSP4 of porcine reproductive and respiratory syndrome virus.BMC veterinary research · 2025Article
- Identification of compounds targeting porcine reproductive and respiratory syndrome virus nsp3 and evaluation of their antiviral efficacy.Virulence · 2025Article
- Understanding the mechanisms of mitochondrial rewiring during viral infections.The Journal of general virology · 2025Review
- Equine lentivirus Gag protein degrades mitochondrial antiviral signaling protein via the E3 ubiquitin ligase Smurf1.Journal of virology · 2025Article
- Review
- Targeting PRMT7-mediated monomethylation of MAVS enhances antiviral innate immune responses and inhibits RNA virus replication.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A Comprehensive Review on Porcine Reproductive and Respiratory Syndrome Virus with Emphasis on Immunity.Vaccines · 2024Review
- Review
- Ursonic acid from medicinal herbs inhibits PRRSV replication through activation of the innate immune response by targeting the phosphatase PTPN1.Veterinary research · 2024Article
- Article
- Construction of an infectious cloning system of porcine reproductive and respiratory syndrome virus and identification of glycoprotein 5 as a potential determinant of virulence and pathogenicity.Frontiers in microbiology · 2023Article
- A New Long Noncoding RNA, MAHAT, Inhibits Replication of Porcine Reproductive and Respiratory Syndrome Virus by Recruiting DDX6 To Bind toJournal of virology · 2022Article
- Tembusu Virus Nonstructural Protein 2B Antagonizes Type I Interferon Production by Targeting MAVS for Degradation.Journal of virology · 2022Article
- Porcine reproductive and respiratory syndrome virus nsp4 positively regulates cellular cholesterol to inhibit type I interferon production.Redox biology · 2022Article
- Evasion of interferon-mediated immune response by arteriviruses.Frontiers in immunology · 2022Review
- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome, a highly infectious disease caused by porcine reproductive and respiratory syndrome virus (PRRSV), has developed various strategies to evade the host innate immune response, including the suppression of type I IFN activation. The mitochondrial antiviral signalling protein (MAVS) is an important bridging adaptor of retinoic acid-inducible gene I/melanoma differentiation-associated protein 5 signalling pathways. Here, we demonstrated that the 3C-like protease (3CLSP) of PRRSV prevented the induction of IFN-β by cleaving MAVS in a proteasome- and caspase-independent manner. Moreover, this cleavage ability was dependent on the protease activity of 3CLSP. Mutations specifically disrupting the cysteine protease activity of 3CLSP eliminated MAVS cleavage and the inhibition of IFN induction. Subsequently, we determined that 3CLSP cleaved MAVS at Glu268. Remarkably, a MAVS point mutation at Glu268 rendered MAVS resistant to 3CLSP cleavage. These results reveal a novel PRRSV mechanism to escape host immunity by directly cleaving MAVS.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.