Ontology highlight
ABSTRACT:
PROVIDER: PRJNA683639 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:While critical for host defense, innate immune cells are also pathologic drivers of acute respiratory distress syndrome (ARDS). Innate immune dynamics during COVID-19 ARDS, compared to ARDS from other respiratory pathogens, is unclear. Moreover, mechanisms underlying beneficial effects of dexamethasone during severe COVID-19 remain elusive. Using scRNA-seq and plasma proteomics, we discovered that compared to bacterial ARDS, COVID-19 was associated with expansion of distinct neutrophil states characterized by interferon (IFN) and prostaglandin (PG) signalling. Dexamethasone during severe COVID-19 depleted circulating neutrophils, altered IFNactive neutrophils, downregulated interferon-stimulated gene, and activated IL1R2+ve neutrophils. Dexamethasone also expanded immunosuppressive immature neutrophils and remodeled cellular interactions by changing neutrophils from information receivers into information providers. Male patients had higher proportions of IFNactive neutrophils, preferential steroid-induced immature neutrophil expansion, and possibly different effects on outcome. Our single-cell atlas (www.biernaskielab.ca/COVID_neutrophil) defines COVID-19-enriched neutrophil states and molecular mechanisms of dexamethasone action to develop targeted immunotherapies for severe COVID-19.
2021-10-05 | GSE157789 | GEO
Project description:The recovery of other pathogens in COVID-19 patients has been reported. The presence of either co-infection or superinfection with bacterial pathogens was associated with poor outcomes, including increased mortality. The recognition of possibility of SARS-CoV-2 co-infection is important as it enables the implementation of appropriate infection control measures and therapy. This is a proof-of-concept study uses in vitro approaches (including crystal violet assay, microrheology, and LC-MS-based prote-omics) to investigate the interaction between SARS-CoV-2 and biofilms of bacteria (S. pneumoniae and S. aureus). SARS-CoV-2 spike protein S1 subunit was found to suppress biofilm formation of both bacteria. The effect of coronavirus and spike protein on bac-terial biofilm was supported by proteomics data that shows variations in proteins in-volved in quorum sensing and biofilm formation/maturation. Preliminary in vitro data suggest that dispersion of opportunistic pathogens from biofilm may be associated with poor prognosis in co-infections. However, further investigations are needed to establish bacterial biofilm as a risk factor for secondary pneumonia in COVID-19 patients.
2022-04-04 | PXD029967 | Pride
Project description:Lung transplantation can potentially be a life-saving treatment for patients with non-resolving COVID-19-associated respiratory failure. Concerns limiting transplant include recurrence of SARS-CoV-2 infection in the allograft, technical challenges imposed by viral-mediated injury to the native lung, and potential risk for allograft infection by pathogens associated with ventilator-associated pneumonia in the native lung. Most importantly, the native lung might recover, resulting in long-term outcomes preferable to transplant. Here, we report results of the first successful lung transplantation procedures in patients with non-resolving COVID-19-associated respiratory failure in the United States. We performed sm-FISH to detect both positive and negative strands of SARS-CoV-2 RNA in the explanted lung tissue, extracellular matrix imaging using SHIELD tissue clearance, and single cell RNA-Seq on explant and warm post-mortem lung biopsies from patients who died from severe COVID-19 pneumonia. Lungs from patients with prolonged COVID-19 were free of virus but pathology showed extensive evidence of injury and fibrosis which resembled end-stage pulmonary fibrosis. We used a machine learning approach to project single cell RNA-Seq data from patients with late stage COVID-19 onto a single cell atlas of pulmonary fibrosis, revealing similarities across cell lineages. There was no recurrence of SARS-CoV-2 or pathogens associated with pre-transplant ventilator associated pneumonias following transplantation. Our findings suggest that some patients with severe COVID-19 develop fibrotic lung disease for which lung transplantation is the only option for survival.
2020-10-28 | GSE158127 | GEO
Project description:High throughput sequencing is performed on mRNA isolated from whole blood of adult Covid-19 patients, bacterial coinfection with Covid-19 and healthy controls in a South Indian cohort. Samples were collected from individuals at the time of hospitalization or visit to clinic. The Covid-19 samples are categorized by severeity.
2022-02-22 | GSE196822 | GEO
Project description:The coronavirus pandemic (COVID-19) is associated with secondary bacterial and fungal infections globally. In India, inappropriate use of glucocorticoids, high prevalence of diabetes mellitus and a conducive environment for fungal growth are considered as the main factors for increased incidence of COVID-19 associated mucormycosis (CAM). Few cases of CAM without steroid abuse and normal blood glucose levels were also reported during the pandemic. This study was designed to explore whether altered immune responses due to severe COVID-19 infection predisposes towards development of mucormycosis. The global transcriptome profiling of monocytes and granulocytic cells derived from CAM, Mucormycosis, COVID-19 and healthy control groups were performed to identify the differentially expressed genes (DEGs) involved in dysregulated host immune response towards respective diseased and healthy conditions.
2024-02-09 | GSE226677 | GEO
Project description:Infection rates involving bacterial and viral pathogens have increased precipitously after the COVID-19 pandemic. While it has been speculated that higher infection rates resulted from increased hospitalizations throughout the pandemic or greater use of antibiotics, precisely why rates remain high today has remained unexplained. Mitochondrial dysfunction is known to occur post-COVID and may disrupt immune responses. Within T cells, SARS-CoV-2 infection is linked to low mitochondrial membrane potential, increased mitochondrial apoptosis, and decreased mitochondrial respiration, which together impact cellular activation and function beyond the acute phase of illness. Here, we demonstrate that decreased mitochondrial function in T cells post-COVID may contribute to higher infection susceptibility by metabolically immobilizing T cell memory responses. Using donor-matched peripheral blood samples from 31 COVID-naïve individuals who subsequently contracted COVID-19, we tracked how influenza A (IAV), Staphylococcus aureus (SA), and Varicella-zoster virus (VZV) T memory cell responses are impacted by COVID-19 infection. We found that gene expression linked to T cell activation decreased but mitochondrial redox-pathway genes increased in CD4 memory T cells post-COVID. However, mitochondrial flux and reactive oxygen species production were limited in a plurality of post-COVID memory T cells after stimulation with IAV, SA, and VZV. Furthermore, we found a disordered relationship between memory T cell mobilization of glycolysis, fatty acid metabolism, and oxidative phosphorylation pathways post-COVID which was partially rescued by pharmacological activation of mitochondrial pathways within antigen-specific T cells. Collectively, these findings indicate that COVID-19 infection may have lasting effects on inhibiting T cell memory responses to commonly encountered community-acquired pathogens, with significant implications for the clinical care of immunologically vulnerable populations in the post-pandemic era.
2026-01-10 | GSE312633 | GEO
Project description:To elucidate key pathways in the host transcriptome of patients infected with SARS-CoV-2, we used RNA sequencing (RNA Seq) to analyze nasopharyngeal (NP) swab and whole blood (WB) samples from 333 COVID-19 patients and controls, including patients with other viral and bacterial infections. Analyses of differentially expressed genes (DEGs) and pathways was performed relative to other infections (e.g. influenza, other seasonal coronaviruses, bacterial sepsis) in both NP swabs and WB. Comparative COVID-19 host responses between NP swabs and WB were examined. Both hospitalized patients and outpatients exhibited upregulation of interferon-associated pathways, although heightened and more robust inflammatory and immune responses were observed in hospitalized patients with more clinically severe disease. A two-layer machine learning-based classifier, run on an independent test set of NP swab samples, was able to discriminate between COVID-19 and non-COVID-19 infectious or non-infectious acute respiratory illness using complete (>1,000 genes), medium (<100) and small (<20) gene biomarker panels with 85.1%-86.5% accuracy, respectively. These findings demonstrate that SARS-CoV-2 infection has a distinct biosignature that differs between NP swabs and WB and can be leveraged for differential diagnosis of COVID-19 disease.
2020-12-15 | GSE163151 | GEO
Project description:Infection by SARS-CoV-2 and subsequent COVID-19 can cause viral sepsis and septic shock. Our past studies demonstrated that dysregulated systemic proteolysis is associated with the pathological mechanism in bacterial septic shock. Thus, here we perform shotgun proteomics and peptidomics analysis by LC-MS/MS to identify and quantify the circulating protein and peptide profile of COVID-19 patient plasma. Plasma samples from four COVID-19 patients were collected at different time points of their ICU stay, including samples from a patient with COVID-19-induced sepsis and bacterial superinfection. By combining mass spectrometry analysis with enzymatic activity assays, our study elucidates the possible pathological involvement of proteolysis in COVID-19-induced sepsis, with particular insight into the dyregulation of protease-mediated systems, such as the coagulation cascade.
2023-03-10 | PXD029181 | Pride
Project description:Post-acute sequelae of COVID-19 (PASC) represent an emerging global crisis. However, quantifiable risk-factors for PASC and their biological associations are poorly resolved. We executed a deep multi-omic, longitudinal investigation of 309 COVID-19 patients from initial diagnosis to convalescence (2-3 months later), integrated with clinical data, and patient-reported symptoms. We resolved four PASC-anticipating risk factors at the time of initial COVID-19 diagnosis: type 2 diabetes, SARS-CoV-2 RNAemia, Epstein-Barr virus viremia, and specific autoantibodies. In patients with gastrointestinal PASC, SARS-CoV-2-specific and CMV-specific CD8+ T cells exhibited unique dynamics during recovery from COVID-19. Analysis of symptom-associated immunological signatures revealed coordinated immunity polarization into four endotypes exhibiting divergent acute severity and PASC. We find that immunological associations between PASC factors diminish over time leading to distinct convalescent immune states. Detectability of most PASC factors at COVID-19 diagnosis emphasizes the importance of early disease measurements for understanding emergent chronic conditions and suggests PASC treatment strategies.
2022-02-01 | E-MTAB-10129 | biostudies-arrayexpress
Project description:A subset of individualsenrolledina randomised controlled trial ofChAdOx1 nCoV-19 and received either ChAdOx1 COVID-19 or control MenACWY vaccine whoexperienced COVID-19-associated symptoms were evaluated using multi-omictechnologies. Participants were selected to represent symptomatic individuals with and without COVID-19 as determined by a nucleic acid amplification test (NAAT) for stage 1 and only NAAT+ve for stage 2 of the study.
2024-03-04 | GSE228841 | GEO