ArticlePLoS pathogens2023
SARS-CoV-2 Nsp8 suppresses MDA5 antiviral immune responses by impairing TRIM4-mediated K63-linked polyubiquitination.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- Herpesviruses and autophagy: An intracellular conflict.Virulence · 2026Review
- Host OTUB2 and viral PLpro stabilize NSP8 to promote SARS-CoV-2 replication.Virologica Sinica · 2026Article
- Disentangling Shared and Differential Genetic Architectures Between COVID-19 and Other Respiratory Disorders-A Genome-Wide Multi-Omics Framework.International journal of molecular sciences · 2026Article
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Dietary Glycerol Monolaurate Enhances Growth and Immune Function in Calves via Hepatic Immunometabolic Reprogramming.Veterinary sciences · 2026Article
- SARS-CoV-2 Nsp1 suppresses the canonical NF-κB pathway by promoting ubiquitin-dependent degradation of TAK1 kinase.PLoS pathogens · 2026Article
- E3 ubiquitin ligase NEDD4 inhibits PEDV infection through ubiquitination and degradation of the viral primase NSP8.Journal of virology · 2026Article
- SARS-CoV-2 NSP8-Derived Peptide Effectively Suppresses the Activity of Helicase NSP13.Computational and structural biotechnology journal · 2026Article
- Article
- Nuclear shuttling of CDC4 mediated broad-spectrum antiviral activity against diverse coronaviruses.Emerging microbes & infections · 2025Article
- SARS-CoV-2 innate immune recognition and implications for respiratory health.Cytokine & growth factor reviews · 2025Review
- Functional and genomic evaluation of novel exopolysaccharide produced by marine Pediococcus pentosaceus E3 with antidiabetic, anticancer, and anti-inflammatory potentials.BMC microbiology · 2025Article
- 4D-DIA Proteomic Analysis of IPEC-J2 Cells Infected with Porcine Group A Rotavirus G9P[23] Strain.Veterinary sciences · 2025Article
- Mitochondrial Reactive Oxygen Species: A Unifying Mechanism in Long COVID and Spike Protein-Associated Injury: A Narrative Review.Biomolecules · 2025Review
- White spot syndrome virus immediate-early protein (wsv100) antagonizes the NF-κB pathway to inhibit innate immune response in shrimp.PLoS pathogens · 2025Article
- RIPK1: A Promising Target for Intervention Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Article
- Impact of SARS-CoV-2 Wuhan and Omicron Variant Proteins on Type I Interferon Response.Viruses · 2025Article
- SARS-CoV-2 infection primes cross-protective respiratory IgA in a MyD88- and MAVS-dependent manner.NPJ vaccines · 2025Article
- Novel Strategies to Profile SARS-CoV-2 and Human Lung Proteome: Inflammatory Pathways in the Spotlight.BioMed research international · 2025Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma differentiation-associated gene-5 (MDA5) acts as a cytoplasmic RNA sensor to detect viral dsRNA and mediates antiviral innate immune responses to infection by RNA viruses. Upon recognition of viral dsRNA, MDA5 is activated with K63-linked polyubiquitination and then triggers the recruitment of MAVS and activation of TBK1 and IKKα/β, subsequently leading to IRF3 and NF-κB phosphorylation. However, the specific E3 ubiquitin ligase for MDA5 K63-polyubiquitination has not been well characterized. Great numbers of symptomatic and severe infections of SARS-CoV-2 are spreading worldwide, and the poor efficacy of treatment with type I interferon and antiviral immune agents indicates that SARS-CoV-2 escapes from antiviral immune responses via several unknown mechanisms. Here, we report that SARS-CoV-2 nonstructural protein 8 (nsp8) acts as a suppressor of antiviral innate immune and inflammatory responses to promote infection of SARS-CoV-2. It downregulates the expression of type I interferon, IFN-stimulated genes and proinflammatory cytokines by binding to MDA5 and TRIM4 and impairing TRIM4-mediated MDA5 K63-linked polyubiquitination. Our findings reveal that nsp8 mediates innate immune evasion during SARS-CoV-2 infection and may serve as a potential target for future therapeutics for SARS-CoV-2 infectious diseases.
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