ArticleJournal of virology2010
Transcriptomic analysis reveals a mechanism for a prefibrotic phenotype in STAT1 knockout mice during severe acute respiratory syndrome coronavirus infection.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- A chemokine gene expression signature derived from meta-analysis predicts the pathogenicity of viral respiratory infections.BMC systems biology · 2011Pooled it
- Role of STAT1 in modulating the host immune response toMicrobiology spectrum · 2026Article
- Article
- Crowdsourcing temporal transcriptomic coronavirus host infection data: Resources, guide, and novel insights.Biology methods & protocols · 2023Article
- 3D Bioprinted Neural-Like Tissue as a Platform to Study Neurotropism of Mouse-Adapted SARS-CoV-2.Advanced biology · 2022Article
- Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Induction of alarmin S100A8/A9 mediates activation of aberrant neutrophils in the pathogenesis of COVID-19.Cell host & microbe · 2021Article
- Immunopathogenesis of Coronavirus-Induced Acute Respiratory Distress Syndrome (ARDS): Potential Infection-Associated Hemophagocytic Lymphohistiocytosis.Clinical microbiology reviews · 2020Review
- SARS-CoV-2 infection-induced immune responses: Friends or foes?Scandinavian journal of immunology · 2020Review
- Type I and Type III Interferons - Induction, Signaling, Evasion, and Application to Combat COVID-19.Cell host & microbe · 2020Review
- A Dangerous Consequence of the Recent Pandemic: Early Lung Fibrosis Following COVID-19 Pneumonia - Case Reports.Therapeutics and clinical risk management · 2020Article
- A tug-of-war between severe acute respiratory syndrome coronavirus 2 and host antiviral defence: lessons from other pathogenic viruses.Emerging microbes & infections · 2020Review
- Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology.Seminars in immunopathology · 2017Review
- The role of epidermal growth factor receptor (EGFR) signaling in SARS coronavirus-induced pulmonary fibrosis.Antiviral research · 2017Review
- Overactive Epidermal Growth Factor Receptor Signaling Leads to Increased Fibrosis after Severe Acute Respiratory Syndrome Coronavirus Infection.Journal of virology · 2017Article
- Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice.Cell host & microbe · 2016Article
- A molecular arms race between host innate antiviral response and emerging human coronaviruses.Virologica Sinica · 2016Review
- Role of signal transducer and activator of transcription 1 in murine allergen-induced airway remodeling and exacerbation by carbon nanotubes.American journal of respiratory cell and molecular biology · 2015Article
- Development of animal models against emerging coronaviruses: From SARS to MERS coronavirus.Virology · 2015Review
- Fc receptors and their influence on efficacy of therapeutic antibodies for treatment of viral diseases.Expert review of anti-infective therapy · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) infection can cause the development of severe end-stage lung disease characterized by acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. The mechanisms by which pulmonary lesions and fibrosis are generated during SARS-CoV infection are not known. Using high-throughput mRNA profiling, we examined the transcriptional response of wild-type (WT), type I interferon receptor knockout (IFNAR1-/-), and STAT1 knockout (STAT1-/-) mice infected with a recombinant mouse-adapted SARS-CoV (rMA15) to better understand the contribution of specific gene expression changes to disease progression. Despite a deletion of the type I interferon receptor, strong expression of interferon-stimulated genes was observed in the lungs of IFNAR1-/- mice, contributing to clearance of the virus. In contrast, STAT1-/- mice exhibited a defect in the expression of interferon-stimulated genes and were unable to clear the infection, resulting in a lethal outcome. STAT1-/- mice exhibited dysregulation of T-cell and macrophage differentiation, leading to a TH2-biased immune response and the development of alternatively activated macrophages that mediate a profibrotic environment within the lung. We propose that a combination of impaired viral clearance and T-cell/macrophage dysregulation causes the formation of prefibrotic lesions in the lungs of rMA15-infected STAT1-/- mice.
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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.