ArticleJournal of virology2005
Inhibition of Beta interferon induction by severe acute respiratory syndrome coronavirus suggests a two-step model for activation of interferon regulatory factor 3.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
196 citing papers in PubMed, 1 synthesis or guideline pooled it, 285 citations in OpenAlex.
- Cell-Mediated Immune Responses to COVID-19 Infection.Frontiers in immunology · 2020Pooled it
- Relationship between gene expression patterns from nasopharyngeal swabs and serum biomarkers in patients hospitalized with COVID-19, following treatment with the neutralizing monoclonal antibody bamlanivimab.Journal of translational medicine · 2022Trial
- Opposing Association of Lung Neutrophils and PD-L1Aging cell · 2026Article
- The inflammation-immunosuppression loop as a driver of immune dysfunction and secondary infections in severe COVID-19.Frontiers in immunology · 2026Review
- The Key to Increase Immunogenicity of Next-Generation COVID-19 Vaccines Lies in the Inclusion of the SARS-CoV-2 Nucleocapsid Protein.Journal of immunology research · 2024Review
- The role of dendritic cells in COVID-19 infection.Emerging microbes & infections · 2023Review
- Differential Type-I Interferon Response in Buffy Coat Transcriptome of Individuals Infected with SARS-CoV-2 Gamma and Delta Variants.International journal of molecular sciences · 2023Article
- Add fuel to the fire: Inflammation and immune response in lung cancer combined with COVID-19.Frontiers in immunology · 2023Review
- A Review of Antibiotic Efficacy in COVID-19 Control.Journal of immunology research · 2023Review
- Article
- Inflammasomes and IL-1 family cytokines in SARS-CoV-2 infection: from prognostic marker to therapeutic agent.Cytokine · 2022Review
- Roles of RNA Sensors in Host Innate Response to Influenza Virus and Coronavirus Infections.International journal of molecular sciences · 2022Review
- Host-Genome Similarity Characterizes the Adaption of SARS-CoV-2 to Humans.Biomolecules · 2022Article
- The SARS-CoV2 and mitochondria: the impact on cell fate.Acta bio-medica : Atenei Parmensis · 2022Review
- Significantly Reduced Retinol Binding Protein 4 (RBP4) Levels in Critically Ill COVID-19 Patients.Nutrients · 2022Observational
- Myeloid-derived suppressor cells in COVID-19: A review.Clinical immunology (Orlando, Fla.) · 2022Review
- Insights into the Role of Neutrophils and Neutrophil Extracellular Traps in Causing Cardiovascular Complications in Patients with COVID-19: A Systematic Review.Journal of clinical medicine · 2022Review
- Mutations in SARS-CoV-2 variants of concern link to increased spike cleavage and virus transmission.Cell host & microbe · 2022Article
- Human airway lineages derived from pluripotent stem cells reveal the epithelial responses to SARS-CoV-2 infection.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Viral deubiquitinases and innate antiviral immune response in livestock and poultry.The Journal of veterinary medical science · 2022Review
136 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus termed SARS-CoV. We and others have previously shown that the replication of SARS-CoV can be suppressed by exogenously added interferon (IFN), a cytokine which is normally synthesized by cells as a reaction to virus infection. Here, we demonstrate that SARS-CoV escapes IFN-mediated growth inhibition by preventing the induction of IFN-beta. In SARS-CoV-infected cells, no endogenous IFN-beta transcripts and no IFN-beta promoter activity were detected. Nevertheless, the transcription factor interferon regulatory factor 3 (IRF-3), which is essential for IFN-beta promoter activity, was transported from the cytoplasm to the nucleus early after infection with SARS-CoV. However, at a later time point in infection, IRF-3 was again localized in the cytoplasm. By contrast, IRF-3 remained in the nucleus of cells infected with the IFN-inducing control virus Bunyamwera delNSs. Other signs of IRF-3 activation such as hyperphosphorylation, homodimer formation, and recruitment of the coactivator CREB-binding protein (CBP) were found late after infection with the control virus but not with SARS-CoV. Our data suggest that nuclear transport of IRF-3 is an immediate-early reaction to virus infection and may precede its hyperphosphorylation, homodimer formation, and binding to CBP. In order to escape activation of the IFN system, SARS-CoV appears to block a step after the early nuclear transport of IRF-3.
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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.