Similar Datasets
Project description:The SARS-CoV-2 has already caused over 523 million COVID-19 cases and 6.27 million deaths worldwide. COVID-19 leads to a severe acute respiratory syndrome, a hyperinflammatory response, and widespread multi-organ damage. Common symptoms of COVID-19 include fever, cough, fatigue, shortness of breath, and loss of taste and smell. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2. We performed RNA-seq analysis of lung tissues from three COVID-19 patients.
2022-09-07 | GSE203401 | GEO
Project description:In this study, we utilized spatial transcriptional assays (NanoString CosMx) to analyze both explant and autopsy samples from non-COVID and COVID-19 lungs, identifying activation of proinflammatory macrophages. We then created macrophage-alveolar and macrophage-airway organoid models, integrating hPSC-derived macrophages with alveolar or airway organoids, and discovered that proinflammatory macrophages induce lung cell senescence through via the THBS1-(ITGA3+ITGB1) pathway. This study not only establishes immune-lung organoid models for studying macrophage-mediated host damage but also highlights the previously unrecognized role of the THBS1-(ITGA3+ITGB1) pathway in lung cell senescence during infectious diseases.
2025-11-14 | GSE287113 | GEO
Project description:In this study, we utilized spatial transcriptional assays (NanoString CosMx) to analyze both explant and autopsy samples from COVID and non-COVID-19 lungs, identifying activation of proinflammatory macrophages. We then created macrophage-alveolar and macrophage-airway organoid models, integrating hPSC-derived macrophages with alveolar or airway organoids, and discovered that proinflammatory macrophages induce lung cell senescence through via the THBS1-(ITGA3+ITGB1) pathway. This study not only establishes immune-lung organoid models for studying macrophage-mediated host damage but also highlights the previously unrecognized role of the THBS1-(ITGA3+ITGB1) pathway in lung cell senescence during infectious diseases.
2025-11-14 | GSE287111 | GEO
Project description: In this study, we elucidated defective viral genome generation in SARS-CoV-2 and its relationship with host antiviral immune response. We observed DVGs ubiquitously from RNA-seq datasets of in vitro infections and autopsy lung tissues of COVID-19 patients.
2023-07-05 | GSE222381 | GEO
Project description:The SARS-CoV-2 pandemic has caused over 1 million deaths globally, mostly due to acute lung injury and acute respiratory distress syndrome, or direct complications resulting in multiple-organ failures. Little is known about the host tissue immune and cellular responses associated with COVID-19 infection, symptoms, and lethality. To address this, we collected tissues from 11 organs during the clinical autopsy of 17 individuals who succumbed to COVID-19, resulting in a tissue bank of approximately 420 specimens. We generated comprehensive cellular maps capturing COVID-19 biology related to patients’ demise through single-cell and single-nucleus RNA-Seq of lung, kidney, liver and heart tissues, and further contextualized our findings through spatial RNA profiling of distinct lung regions. We developed a computational framework that incorporates removal of ambient RNA and automated cell type annotation to facilitate comparison with other healthy and diseased tissue atlases. In the lung, we uncovered significantly altered transcriptional programs within the epithelial, immune and stromal compartments and cell intrinsic changes in multiple cell types relative to lung tissue from healthy controls. We observed evidence of alveolar type 2 (AT2) differentiation replacing depleted alveolar type 1 (AT1) lung epithelial cells, as previously seen in fibrosis, and a concomitant increase in myofibroblasts reflective of defective tissue repair. Viral reads were enriched in lung mononuclear phagocytic cells and endothelial cells, and these cells expressed distinct viral RNA host response transcriptional programs. We corroborated the compositional and transcriptional changes in lung tissue through spatial analysis of RNA profiles in situ and distinguished unique tissue host responses between regions with and without viral RNA, and in COVID-19 donor tissues relative to healthy lung. Finally, we analyzed genetic regions implicated in COVID-19 GWAS with transcriptomic data to implicate specific cell types and genes associated with disease severity. Overall, our COVID-19 cell atlas is a foundational dataset to better understand the biological impact of SARS-CoV-2 infection across the human body and empowers the identification of new therapeutic interventions and prevention strategies.
2021-04-11 | GSE163529 | GEO
Project description:Male sex belongs to one of the risk factors for severe COVID-19 outcome. However, underlying mechanisms that could affect sex dependent disease outcome are yet unknown. Here, we identified the CYP19A1 gene encoding for the testosterone-to-estradiol metabolizing enzyme CYP19A1 (alias aromatase) as a host factor that contributes to worsened disease outcome in male hamsters. SARS-CoV-2 infection increases CYP19A1 transcription most prominently in the lungs of male animals, which correlates with reduced circulating testosterone and increased circulating estradiol levels. Dysregulated sex hormone levels in male golden hamsters are associated with reduced lung function compared to females. Treatment of SARS-CoV-2 infected hamsters with letrozole, a clinically approved CYP19A1 inhibitor, supported recovery of dysregulated sex hormone levels and was associated with improved lung function in male but not female animals compared to placebo controls. Whole-lung transcriptome analysis in letrozole treated versus placebo treated control groups revealed key pathways associated with improved lung health in males. To seek translation of these findings into humans, we analyzed autopsy-derived lung samples of COVID-19 cases from three independent study sites. We found that CYP19A1 transcription and protein expression is strongly elevated in the lungs of men who died with COVID-19 as compared to females or non-COVID-19 controls. Our findings highlight the role of the lung as a yet unrecognized but critical organ involved in metabolic responses against respiratory virus infections. Furthermore, inhibition of CYP19A1 by the clinically approved drug letrozole may pose a new therapeutic strategy to reduce poor long-term COVID-19 outcome.
2022-01-21 | E-MTAB-11162 | biostudies-arrayexpress
Project description:The SARS-CoV-2 pandemic has caused over 1 million deaths globally, mostly due to acute lung injury and acute respiratory distress syndrome, or direct complications resulting in multiple-organ failures. Little is known about the host tissue immune and cellular responses associated with COVID-19 infection, symptoms, and lethality. To address this, we collected tissues from 11 organs during the clinical autopsy of 17 individuals who succumbed to COVID-19, resulting in a tissue bank of approximately 420 specimens. We generated comprehensive cellular maps capturing COVID-19 biology related to patients’ demise through single-cell and single-nucleus RNA-Seq of lung, kidney, liver and heart tissues, and further contextualized our findings through spatial RNA profiling of distinct lung regions. We developed a computational framework that incorporates removal of ambient RNA and automated cell type annotation to facilitate comparison with other healthy and diseased tissue atlases. In the lung, we uncovered significantly altered transcriptional programs within the epithelial, immune and stromal compartments and cell intrinsic changes in multiple cell types relative to lung tissue from healthy controls. We observed evidence of alveolar type 2 (AT2) differentiation replacing depleted alveolar type 1 (AT1) lung epithelial cells, as previously seen in fibrosis, and a concomitant increase in myofibroblasts reflective of defective tissue repair. Viral reads were enriched in lung mononuclear phagocytic cells and endothelial cells, and these cells expressed distinct viral RNA host response transcriptional programs. We corroborated the compositional and transcriptional changes in lung tissue through spatial analysis of RNA profiles in situ and distinguished unique tissue host responses between regions with and without viral RNA, and in COVID-19 donor tissues relative to healthy lung. Finally, we analyzed genetic regions implicated in COVID-19 GWAS with transcriptomic data to implicate specific cell types and genes associated with disease severity. Overall, our COVID-19 cell atlas is a foundational dataset to better understand the biological impact of SARS-CoV-2 infection across the human body and empowers the identification of new therapeutic interventions and prevention strategies.
2021-04-11 | GSE164013 | GEO
Project description:The SARS-CoV-2 pandemic has caused over 1 million deaths globally, mostly due to acute lung injury and acute respiratory distress syndrome, or direct complications resulting in multiple-organ failures. Little is known about the host tissue immune and cellular responses associated with COVID-19 infection, symptoms, and lethality. To address this, we collected tissues from 11 organs during the clinical autopsy of 17 individuals who succumbed to COVID-19, resulting in a tissue bank of approximately 420 specimens. We generated comprehensive cellular maps capturing COVID-19 biology related to patients’ demise through single-cell and single-nucleus RNA-Seq of lung, kidney, liver and heart tissues, and further contextualized our findings through spatial RNA profiling of distinct lung regions. We developed a computational framework that incorporates removal of ambient RNA and automated cell type annotation to facilitate comparison with other healthy and diseased tissue atlases. In the lung, we uncovered significantly altered transcriptional programs within the epithelial, immune and stromal compartments and cell intrinsic changes in multiple cell types relative to lung tissue from healthy controls. We observed evidence of alveolar type 2 (AT2) differentiation replacing depleted alveolar type 1 (AT1) lung epithelial cells, as previously seen in fibrosis, and a concomitant increase in myofibroblasts reflective of defective tissue repair. Viral reads were enriched in lung mononuclear phagocytic cells and endothelial cells, and these cells expressed distinct viral RNA host response transcriptional programs. We corroborated the compositional and transcriptional changes in lung tissue through spatial analysis of RNA profiles in situ and distinguished unique tissue host responses between regions with and without viral RNA, and in COVID-19 donor tissues relative to healthy lung. Finally, we analyzed genetic regions implicated in COVID-19 GWAS with transcriptomic data to implicate specific cell types and genes associated with disease severity. Overall, our COVID-19 cell atlas is a foundational dataset to better understand the biological impact of SARS-CoV-2 infection across the human body and empowers the identification of new therapeutic interventions and prevention strategies.
2021-04-11 | GSE162911 | GEO
Project description:Transcriptional response to SARS-CoV-2 infection in human autopsy lung samples
| PRJNA822828 | ENA