ArticleCell & bioscience2022
SARS-CoV-2 NSP13 helicase suppresses interferon signaling by perturbing JAK1 phosphorylation of STAT1.
Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- Recent advances in functional studies of coronavirus NSP13 helicase and challenges in inhibitor development.Virulence · 2026Review
- Comparative innate immune responses across major RNA and DNA viral infections: Mechanisms, immunopathology, and therapeutic perspectives.Human vaccines & immunotherapeutics · 2026Review
- Repurposing drug screen for the identification of helicase inhibitors from viruses of pandemic concern.SLAS discovery : advancing life sciences R & D · 2026Article
- Review
- Modulation of Host Innate Immune Response by Highly Pathogenic Human Coronaviruses during Viral Infection.Journal of microbiology and biotechnology · 2026Review
- Dysregulated host miRNAs with antiviral potential against SARS-CoV-2 identified from COVID-19 patients.Journal of translational medicine · 2026Article
- Motif V is an allosteric couple between the SARS-CoV-2 nsp13 nucleotide triphosphatase and helicase active sites.The Journal of biological chemistry · 2026Article
- Rewriting the viral script: post-translational modifications orchestrating SARS-CoV-2 pathogenesis and immune evasion.Frontiers in microbiology · 2026Review
- SARS-CoV-2 NSP8-Derived Peptide Effectively Suppresses the Activity of Helicase NSP13.Computational and structural biotechnology journal · 2026Article
- Structural and Computational Insights into the Attenuated Innate Immune Recognition of the SARS-CoV-2 N15 Lineage, an Early-Pandemic Variant.Computational and structural biotechnology journal · 2026Article
- Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2.Emerging microbes & infections · 2025Article
- The bittersweet link between glucose metabolism, cellular microenvironment and viral infection.Virulence · 2025Review
- The nonstructural protein 13 of porcine deltacoronavirus coordinates ATP-driven duplex unwinding and ATP-independent strand annealing for nucleic acid remodeling.BMC veterinary research · 2025Article
- Impact of SARS-CoV-2 Wuhan and Omicron Variant Proteins on Type I Interferon Response.Viruses · 2025Article
- Anti-interferon armamentarium of human coronaviruses.Cellular and molecular life sciences : CMLS · 2025Review
- Review
- In vitro selection and analysis of SARS-CoV-2 nirmatrelvir resistance mutations contributing to clinical virus resistance surveillance.Science advances · 2024Article
- Progressive Evolutionary Dynamics of Gene-Specific ω Led to the Emergence of Novel SARS-CoV-2 Strains Having Super-Infectivity and Virulence with Vaccine Neutralization.International journal of molecular sciences · 2024Article
- The PKA-CREB1 axis regulates coronavirus proliferation by viral helicase nsp13 association.Journal of virology · 2024Article
- SARS-CoV-2 biology and host interactions.Nature reviews. Microbiology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundSARS-CoV-2 is the causative agent of COVID-19. Overproduction and release of proinflammatory cytokines are the underlying cause of severe COVID-19. Treatment of this condition with JAK inhibitors is a double-edged sword, which might result in the suppression of proinflammatory cytokine storm and the concurrent enhancement of viral infection, since JAK signaling is essential for host antiviral response. Improving the current JAK inhibitor therapy requires a detailed molecular analysis on how SARS-CoV-2 modulates interferon (IFN)-induced activation of JAK-STAT signaling.
resultsIn this study, we focused on the molecular mechanism by which SARS-CoV-2 NSP13 helicase suppresses IFN signaling. Expression of SARS-CoV-2 NSP13 alleviated transcriptional activity driven by type I and type II IFN-responsive enhancer elements. It also prevented nuclear translocation of STAT1 and STAT2. The suppression of NSP13 on IFN signaling occurred at the step of STAT1 phosphorylation. Nucleic acid binding-defective mutant K345A K347A and NTPase-deficient mutant E375A of NSP13 were found to have largely lost the ability to suppress IFN-β-induced STAT1 phosphorylation and transcriptional activation, indicating the requirement of the helicase activity for NSP13-mediated inhibition of STAT1 phosphorylation. NSP13 did not interact with JAK1 nor prevent STAT1-JAK1 complex formation. Mechanistically, NSP13 interacted with STAT1 to prevent JAK1 kinase from phosphorylating STAT1.
conclusionSARS-CoV-2 NSP13 helicase broadly suppresses IFN signaling by targeting JAK1 phosphorylation of STAT1.
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