ArticleFrontiers in immunology2023
Swine acute diarrhoea syndrome coronavirus (SADS-CoV) Nsp5 antagonizes type I interferon signaling by cleaving DCP1A.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Review
- Article
- The coronavirus 3CL protease: Unveiling its complex host interactions and central role in viral pathogenesis.Virologica Sinica · 2025Review
- SADS-CoV nsp5 Inhibits Interferon Production by Targeting Kinase IKKε.Microorganisms · 2025Article
- The Seneca Valley virus 3C protease cleaves DCP1A to attenuate its antiviral effects.Veterinary research · 2025Article
- Interplay of swine acute diarrhoea syndrome coronavirus and the host intrinsic and innate immunity.Veterinary research · 2025Review
- Swine Acute Diarrhea Syndrome Coronavirus: An Overview of Virus Structure and Virus-Host Interactions.Animals : an open access journal from MDPI · 2025Review
- NS7a of SADS-CoV promotes viral infection via inducing apoptosis to suppress type III interferon production.Journal of virology · 2024Article
- Porcine deltacoronavirus nsp5 antagonizes type I interferon signaling by cleaving IFIT3.Journal of virology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Swine acute diarrhoea syndrome coronavirus (SADS-CoV), which is a recently discovered enteric coronavirus, is the major aetiological agent that causes severe clinical diarrhoea and intestinal pathological damage in pigs, and it has caused significant economic losses to the swine industry. Nonstructural protein 5, also called 3C-like protease, cleaves viral polypeptides and host immune-related molecules to facilitate viral replication and immune evasion. Here, we demonstrated that SADS-CoV nsp5 significantly inhibits the Sendai virus (SEV)-induced production of IFN-β and inflammatory cytokines. SADS-CoV nsp5 targets and cleaves mRNA-decapping enzyme 1a (DCP1A) via its protease activity to inhibit the IRF3 and NF-κB signaling pathways in order to decrease IFN-β and inflammatory cytokine production. We found that the histidine 41 and cystine 144 residues of SADS-CoV nsp5 are critical for its cleavage activity. Additionally, a form of DCP1A with a mutation in the glutamine 343 residue is resistant to nsp5-mediated cleavage and has a stronger ability to inhibit SADS-CoV infection than wild-type DCP1A. In conclusion, our findings reveal that SADS-CoV nsp5 is an important interferon antagonist and enhance the understanding of immune evasion by alpha coronaviruses.
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