ArticleMicroorganisms2021
SARS-CoV-2 Nonstructural Proteins 1 and 13 Suppress Caspase-1 and the NLRP3 Inflammasome Activation.
Article in Microorganisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 50 citations in OpenAlex.
- PANoptosis as a Therapeutic Target for COVID-19.Current microbiology · 2026Review
- The Open Reading Frame 7b of the SARS-CoV-2 Disperse Trans-Golgi and Activate the NLRP3 Inflammasome.Journal of medical virology · 2026Article
- Antiviral Inflammasomes and How to Find Them.Viruses · 2026Review
- Pyroptosis in Respiratory Virus Infections: A Narrative Review of Mechanisms, Pathophysiology, and Potential Therapeutic Interventions.Microorganisms · 2025Review
- Activation and evasion of inflammasomes during viral and microbial infection.Cellular and molecular life sciences : CMLS · 2025Review
- Impaired NLRP3 inflammasome signaling diverts pyroptotic to apoptotic caspase activation in macrophages.Frontiers in immunology · 2025Article
- Porcine Epidemic Diarrhea Virus Infection of Porcine Intestinal Epithelial Cells Causes Mitochondrial DNA Release and the Activation of the NLRP3 Inflammasome to Mediate Interleukin-1β Secretion.Veterinary sciences · 2024Article
- Apoptosis and pyroptosis in the nasal mucosa of Syrian hamster during SARS-CoV-2 infection and reinfection.Apoptosis : an international journal on programmed cell death · 2024Article
- New insights into the pathogenesis of SARS-CoV-2 during and after the COVID-19 pandemic.Frontiers in immunology · 2024Review
- Procoagulant Status and Fibrinolytic Activity in COVID-19 Patients during Illness and Convalescence.Biomedicines · 2023Article
- SARS-CoV-2 Papain-like Protease Negatively Regulates the NLRP3 Inflammasome Pathway and Pyroptosis by Reducing the Oligomerization and Ubiquitination of ASC.Microorganisms · 2023Article
- The role of cell death in SARS-CoV-2 infection.Signal transduction and targeted therapy · 2023Review
- SARS-CoV-2 nsp13 Restricts Episomal DNA Transcription without Affecting Chromosomal DNA.Journal of virology · 2023Article
- Review
- Inflammasomes: a rising star on the horizon of COVID-19 pathophysiology.Frontiers in immunology · 2023Review
- Role of NLRP3 inflammasome in diabetes and COVID-19 role of NLRP3 inflammasome in the pathogenesis and treatment of COVID-19 and diabetes NLRP3 inflammasome in diabetes and COVID-19 intervention.Frontiers in immunology · 2023Review
- Inflammasome activation by viral infection: mechanisms of activation and regulation.Frontiers in microbiology · 2023Review
- Race between virus and inflammasomes: inhibition or escape, intervention and therapy.Frontiers in cellular and infection microbiology · 2023Review
- Antiviral Activities of Ethyl Pheophorbides a and b Isolated fromMolecules (Basel, Switzerland) · 2022Article
- Kaempferol Interferes with Varicella-Zoster Virus Replication in Human Foreskin Fibroblasts.Pharmaceuticals (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
Viral infection-induced activation of inflammasome complexes has both positive and negative effects on the host. Proper activation of inflammasome complexes induces down-stream effector mechanisms that inhibit viral replication and promote viral clearance, whereas dysregulated activation has detrimental effects on the host. Coronaviruses, including SARS-CoV and MERS-CoV, encode viroporins that activate the NLRP3 inflammasome, and the severity of coronavirus disease is associated with the inflammasome activation. Although the NLRP3 inflammasome activation is implicated in the pathogenesis of coronaviruses, these viruses must evade inflammasome-mediated antiviral immune responses to establish primary replication. Screening of a complementary DNA (cDNA) library encoding 28 SARS-CoV-2 open reading frames (ORFs) showed that two nonstructural proteins (NSPs), NSP1 and NSP13, inhibited caspase-1-mediated IL-1β activation. NSP1 amino acid residues involved in host translation shutoff and NSP13 domains responsible for helicase activity were associated with caspase-1 inhibition. In THP-1 cells, both NSP1 and NSP13 significantly reduced NLRP3-inflammasome-induced caspase-1 activity and IL-1β secretion. These findings indicate that SARS-CoV-2 NSP1 and NSP13 are potent antagonists of the NLRP3 inflammasome.
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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.