Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA97445 | ENA |
REPOSITORIES: ENA
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Project description:Some patients infected with Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) develop severe pneumonia and the acute respiratory distress syndrome (ARDS). Distinct clinical features in these patients have led to speculation that the immune response to virus in the SARS-CoV-2-infected alveolus differs from other types of pneumonia. We collected bronchoalveolar lavage fluid samples from 88 patients with SARS-CoV-2-induced respiratory failure and 211 patients with known or suspected pneumonia from other pathogens and subjected them to flow cytometry and bulk transcriptomic profiling. We performed single-cell RNA-seq on 10 bronchoalveolar lavage fluid samples collected from patients with severe COVID-19 within 48 hours of intubation. In the majority of patients with SARS-CoV-2 infection, the alveolar space was persistently enriched in T cells and monocytes. Bulk and single-cell transcriptomic profiling suggested that SARS-CoV-2 infects alveolar macrophages, which in turn respond by producing T cell chemoattractants. These T cells produce interferon-gamma to induce inflammatory cytokine release from alveolar macrophages and further promote T cell activation. Collectively, our results suggest that SARS-CoV-2 causes a slowly-unfolding, spatially-limited alveolitis in which alveolar macrophages harboring SARS-CoV-2 and T cells form a positive feedback loop that drives persistent alveolar inflammation.
2020-08-05 | GSE155249 | GEO
Project description:The causative organism, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibits a wide spectrum of clinical manifestations in disease-ridden patients. Differences in the severity of COVID-19 ranges from asymptomatic infections and mild cases to the severe form, leading to acute respiratory distress syndrome (ARDS) and multiorgan failure with poor survival. MiRNAs can regulate various cellular processes, including proliferation, apoptosis, and differentiation, by binding to the 3′UTR of target mRNAs inducing their degradation, thus serving a fundamental role in post-transcriptional repression. Alterations of miRNA levels in the blood have been described in multiple inflammatory and infectious diseases, including SARS-related coronaviruses. We used microarrays to delineate the miRNAs and snoRNAs signature in the peripheral blood of severe COVID-19 cases (n=9), as compared to mild (n=10) and asymptomatic (n=10) patients, and identified differentially expressed transcripts in severe versus asymptomatic, and others in severe versus mild COVID-19 cases. A cohort of 29 male age-matched patients were selected. All patients were previously diagnosed with COVID-19 using TaqPath COVID-19 Combo Kit (Thermo Fisher Scientific, Waltham, Massachusetts), or Cobas SARS-CoV-2 Test (Roche Diagnostics, Rotkreuz, Switzerland), with a CT value < 30. Additional criterion for selection was age between 35 and 75 years. Participants were grouped into severe, mild and asymptomatic. Classifying severe cases was based on requirement of high-flow oxygen support and ICU admission (n=9). Whereas mild patients were identified based on symptoms and positive radiographic findings with pulmonary involvement (n=10). Patients with no clinical presentation were labelled as asymptomatic cases (n=10).
2022-03-01 | E-MTAB-10970 | biostudies-arrayexpress
Project description:The outbreak of Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, has led to an unparalleled global health crisis. While the majority of COVID-19 patients present with mild respiratory issues, a subset of patients still develop severe symptoms and life-threatening complications. Notably, abnormal coagulation and thrombosis are significant contributors to mortality in severe COVID-19 patients. Therefore, this study stimulated aortic endothelial cells with SARS-Cov-2 S protein and performed transcriptome sequencing analysis.
2024-12-15 | GSE283771 | GEO
Project description:In this study, we used blood samples of nine patients with severe SARS-CoV-2 infection either with or without acute respiratory distress syndrome (ARDS) and analyzed them on the Illumina EPIC methylation microarray.
2022-11-15 | GSE161988 | GEO
Project description:Coagulopathy is a hallmark finding in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is associated with an increased risk of death from venous and arterial thromboembolic complications. SARS-CoV-2 infection can lead to microvascular thrombosis that contributes to acute lung injury and respiratory failure. The molecular mechanisms leading to thrombosis in Coronavirus disease 2019 (COVID19) patients are poorly understood. Here, we study a role of the procoagulant neutrophil extracellular traps (NETs)/Factor XII (FXII) axis in COVID19-associated thromboembolism.
2021-08-20 | PXD020216 | Pride
Project description:Coagulopathy is a hallmark finding in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is associated with an increased risk of death from venous and arterial thromboembolic complications. SARS-CoV-2 infection can lead to microvascular thrombosis that contributes to acute lung injury and respiratory failure. The molecular mechanisms leading to thrombosis in Coronavirus disease 2019 (COVID19) patients are poorly understood. Here, we study a role of the procoagulant neutrophil extracellular traps (NETs)/Factor XII (FXII) axis in COVID19-associated thromboembolism.
2021-08-20 | PXD020279 | Pride
Project description:To in-depth analyze the anti-SARS-CoV-2 humoral response and find elements that can lead or prevent acute respiratory distress syndrome (ARDS), we dissected the multiple layers of B cell responses by NGS immunoglobulin repertoires on RNA template from peripheral blood cell of severe COVID-19 patients.
2024-01-08 | GSE222431 | GEO
Project description:Background: The recent emergence of a novel coronavirus in the Middle East (designated MERS-CoV) is a reminder of the zoonotic potential of coronaviruses and the severe disease these etiologic agents can cause in humans. Clinical features of Middle East respiratory syndrome (MERS) include severe acute pneumonia and renal failure that is highly reminiscent of severe acute respiratory syndrome (SARS) caused by SARS-CoV. The host response is a key component of highly pathogenic respiratory virus infection. Here, we computationally analyzed gene expression changes in a human airway epithelial cell line infected with two genetically distinct MERS-CoV strains obtained from human patients, MERS-CoV-EMC (designated EMC) and MERS-CoV-London (designated LoCoV). Results: Using topological techniques, such as persistence homology and filtered clustering, we characterized the host response system to the different MERS-CoVs, with LoCoV inducing early kinetic changes, between 3 and 12 hours post infection, compared to EMC. Robust transcriptional changes distinguished the two MERS-CoV strains predominantly at the late time points. Combining statistical analysis of infection and cytokine-stimulated treatment transcriptomics, we identified differential innate and pro-inflammatory responses between the two virus strains, including up-regulation of extracellular remodeling genes following LoCoV infection and differential pro-inflammatory responses between the two strains. Conclusions: These transcriptional differences may be the result of amino acid differences in viral proteins known to modulate innate immunity against MERS infection. Triplicate wells of Calu-3 2B4 cells were infected with Human Coronavirus EMC 2012 (HCoV-EMC) or time-matched mock infected. Cells were harvested at 0, 3, 7, 12, 18 and 24 hours post-infection (hpi), RNA extracted and transcriptomics analyzed by microarray.
2014-08-31 | E-GEOD-56677 | biostudies-arrayexpress
Project description:The open reading frame (ORF) 8 in severe acute respiratory syndrome coronaviruses (SARS-CoVs), associated with host adaptation and viral replication, is a hotspot for mutation. However, mutation effects on host immune responses remain unknown. Here, whole blood transcriptomics performed on patients infected with mutant SARS-CoV-2 (Δ382; 382-nt deletion in ORF8) show differing profiles from wildtype SARS-CoV-2. Understanding the Δ382 mechanism and effects would allow for a focused approach in vaccine and antiviral development.
2021-04-24 | GSE155454 | GEO