ArticleCellular & molecular immunology2021
SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting IRF3 nuclear translocation.
Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 143 citations in OpenAlex.
- The crucial role of RIG-I in upregulating neutrophil CXCR2 expression through the MAPK signaling pathway in viral pneumonia.Respiratory research · 2026Article
- Modulation of Host Innate Immune Response by Highly Pathogenic Human Coronaviruses during Viral Infection.Journal of microbiology and biotechnology · 2026Review
- Redundant and distinct mechanisms suppress innate immune activation during SARS-CoV-2 infection.PLoS biology · 2026Article
- Inhibiting the interaction between the mitochondrial receptor Tom70 and SARS CoV 2 Orf9b with small molecules.bioRxiv : the preprint server for biology · 2026Article
- SARS-CoV-2 nonstructural protein 3 remodels the phosphorylation of target proteins via protein-protein interactions.Microbiology spectrum · 2026Article
- G3BP1 methylation by PRMT5 facilitates its recruitment of TBK1 for IRF3 activation during host response to foreign ribonucleic acids.Frontiers in immunology · 2026Article
- The inflammation-immunosuppression loop as a driver of immune dysfunction and secondary infections in severe COVID-19.Frontiers in immunology · 2026Review
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
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- 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
- A comprehensive review of current insights into the virulence factors of SARS-CoV-2.Journal of virology · 2025Review
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- Acute COVID-19 and LongCOVID syndrome - molecular implications for therapeutic strategies - review.Frontiers in immunology · 2025Review
- Direct RNA sequencing reveals m6A modifications and isoform changes in SARS-CoV-2-infected HEK cells.Access microbiology · 2025Article
- Viral strategies to antagonize the host antiviral innate immunity: an indispensable research direction for emerging virus-host interactions.Emerging microbes & infections · 2024Review
- MDA5 Is a Major Determinant of Developing Symptoms in Critically Ill COVID-19 Patients.Clinical reviews in allergy & immunology · 2024Review
- MERS-CoV-nsp5 expression in human epithelial BEAS 2b cells attenuates type I interferon production by inhibiting IRF3 nuclear translocation.Cellular and molecular life sciences : CMLS · 2024Article
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
40 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2 is the pathogenic agent of COVID-19, which has evolved into a global pandemic. Compared with some other respiratory RNA viruses, SARS-CoV-2 is a poor inducer of type I interferon (IFN). Here, we report that SARS-CoV-2 nsp12, the viral RNA-dependent RNA polymerase (RdRp), suppresses host antiviral responses. SARS-CoV-2 nsp12 attenuated Sendai virus (SeV)- or poly(I:C)-induced IFN-β promoter activation in a dose-dependent manner. It also inhibited IFN promoter activation triggered by RIG-I, MDA5, MAVS, and IRF3 overexpression. Nsp12 did not impair IRF3 phosphorylation but suppressed the nuclear translocation of IRF3. Mutational analyses suggested that this suppression was not dependent on the polymerase activity of nsp12. Given these findings, our study reveals that SARS-CoV-2 RdRp can antagonize host antiviral innate immunity and thus provides insights into viral pathogenesis.
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Registered trials
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.