Ontology highlight
ABSTRACT:
PROVIDER: PRJNA780093 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16938236_1.fastq.gz | Fastqsanger.gz | |||
| SRR16938236_2.fastq.gz | Fastqsanger.gz | |||
| SRR16938237_1.fastq.gz | Fastqsanger.gz | |||
| SRR16938237_2.fastq.gz | Fastqsanger.gz | |||
| SRR16938238_1.fastq.gz | Fastqsanger.gz |
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Project description:Characterizing cerebrospinal fluid immunity in neurological manifestations of COVID-19
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Project description:Patients suffering from Coronavirus disease 2019 (COVID-19) can develop neurological sequelae, such as headache, neuroinflammatory or cerebrovascular disease. These conditions - here termed Neuro-COVID - are more frequent in patients with severe COVID-19. To understand the etiology of these neurological sequelae, we utilized single-cell sequencing and examined the immune cell profiles from the cerebrospinal fluid (CSF) of Neuro-COVID patients compared to patients with non-inflammatory and autoimmune neurological diseases or with viral encephalitis. The CSF of Neuro-COVID patients exhibited an expansion of dedifferentiated monocytes and of exhausted CD4+ T cells. Neuro-COVID CSF leukocytes featured an enriched interferon signature; however, this was less pronounced than in viral encephalitis. Repertoire analysis revealed broad clonal T cell expansion and curtailed interferon response in severe compared to mild Neuro-COVID patients. Collectively, our findings document the CSF immune compartment in Neuro-COVID patients and suggest compromised antiviral responses in this setting.
2020-12-11 | GSE163005 | GEO
Project description:Background. COVID-19-induced neurological disease is a growing concern. Here we provide a comprehensive clinical, molecular, and neuroimaging investigation of patients presenting neurological symptoms to investigate underlying processes. Methods. We performed a detailed systematized clinical, laboratory, and neuroimaging (CT/MRI) data analysis from 35 mild to severe Brazilian COVID-19 hospitalised patients with clinical indications for cerebrospinal fluid (CSF) exam. In patients' CSF, we measured interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α) and the Alzheimer's disease-associated biomarkers amyloid-beta (Aβ)1-40, Aβ1-42, Tau and pTau181 levels (n=31-35). In addition, CSF proteomics and the search for SARS-CoV-2 spike protein presence using shotgun and targeted multiple reaction monitoring liquid-chromatography/mass-spectrometry were performed (n=16). We further evaluated a 29-cytokine panel in patients’ blood (n=16). An electronic questionnaire was conducted one-year post-hospitalisation (n=19, 63.3%). Findings. COVID-19 patients presented heterogeneous clinical and neurological features, including encephalopathy, encephalitis, and neuromuscular syndromes, despite low pulmonary burden. Patients showed increased circulating cytokines and CSF IL-6 and TNF-α levels compared to controls. Alzheimer’s disease-related biomarkers were unaltered compared to controls. COVID-19 altered CSF proteomic pathways associated to complement and coagulation cascades, immune-inflammatory, metabolism and amyloidosis. We found no traces of spike protein in patients’ CSF. Severe patients presented more pronounced neuroimaging alterations, altered CSF levels of IL-6, Tau, and Aβ-species compared to mild patients. Peripheral inflammation markers correlated with CSF IL-6 and Tau-species levels. Finally, in a one-year post-COVID survey, survivors were not recovered entirely (12/19) and reported confusion or memory/attention deficits (13/19). Interpretation. COVID-19 induces a broad spectrum of neurological presentations associated with changes in central nervous system (CNS) inflammatory and neurodegenerative molecular and structural biomarkers that correlate with systemic inflammation and disease severity. Given that neurological symptoms persist up to one-year post-COVID, our results urge us to investigate whether systemic, and CNS molecular changes are permanent or alleviated so that COVID-19 patients with lingering symptoms are adequately treated.
2024-08-09 | PXD033979 | Pride
Project description:SARS-Cov-2 infection is frequently associated with Nervous System (NS) manifestations. However, it is not clear how SARS-CoV-2 can cause neurological dysfunctions and which molecular processes affects. In this work, we examined the frontal cortex tissue of patients who died of COVID-19 for the presence of SARS-CoV-2, comparing qRT-PCR with ddPCR. We also investigated the transcriptomic profile of frontal cortex from COVID-19 patients and matched controls by RNA-seq analysis to characterize the transcriptional signature.
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Project description:Circulating miRNAs in patients who underwent ARDS and needed mechanical ventilation were analyzed by next generation sequencing (NGS) in comparison with patients who had COVID-19 poor symptoms but without intensive care unit requirement.
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Project description:A novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of COVID-19 and continues to be a global health challenge. To understand viral disease biology, we have carried out proteo-genomic analysis using next generation sequencing (NGS) and mass-spectrometry on nasopharyngeal swabs of COVID-19 patients to examine clinical genome and proteome. Our proteomic analysis, for the first time identified 13 different SARS-CoV-2 proteins from the clinical swabs. Additionally, host proteome analysis revealed several key host proteins to be uniquely expressed in COVID-19 patients. Besides revealing aspects of host-virus pathogenesis, our study opens avenues to develop better diagnostic markers and therapeutic strategies.
2021-06-28 | PXD021896 | Pride
Project description:Extrapulmonary manifestations of COVID-19 have gained attention, not only due to their links to clinical outcomes, but also due to their potential long-term sequelae1. Recent evidence has shown multi-organ tropism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), including heart, kidney and liver2. Previous studies have shown that close to 20% of hospitalized patients with COVID-19 develop liver injury, showing an association to disease severity3. Here, we identified a high frequency of liver enzyme alterations at admission in COVID-19 patients who required hospitalization. Then, we characterized SARS-CoV-2 liver tropism in autopsy samples, based on the expression of cell-entry facilitators in parenchymal cells, clinical polymerase chain reaction (PCR) positivity, subgenomic SARS-CoV-2 identification using RNA sequencing, and viral RNA detection by in situ hybridization. Next, we unraveled the transcriptomic and proteomic landscape of SARS-CoV-2 liver tropism, revealing significant increases in interferon alpha and gamma signaling and compensatory liver-specific metabolic regulation. While these results reflect changes in tissues from patients with severe SARS-CoV-2 infection, these profound molecular alterations raise questions about the potential long-term consequences of COVID-19 infection.
2022-04-02 | PXD022789 | Pride
Project description:Purpose: Recent studies have focused their attention on conjunctivitis as one of the symptoms of coronavirus disease 2019 (COVID-19). Therefore, tear samples were taken from COVID-19 patients and the presence of SARS-CoV-2 was evidenced using Real Time reverse transcription polymerase chain reaction. Methods: The main aim of this study was to analyze mRNA expression in the tears of patients with COVID-19 viral infection compared with healthy subjects using Next Generation Sequencing (NGS). Results: The functional evaluation of the transcriptome highlighted 25 genes that differ statistically between healthy individuals and patients affected by COVID-19 disease. In particular, the NGS analysis identified the presence of several genes involved in B cell signaling and keratinization. In particular, the genes involved in B cell signaling were downregulated in the tears of COVID-19 patients, while those involved in keratinization were upregulated. Conclusions: The results indicated that COVID-19 may induce a process of ocular keratinization and a defective B cell response.
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Project description:We reported a case series of 8 patients with prominent new-onset neurological manifestations, who were screened out from a patch of 304 COVID-19 confirmed patients. Proteomics were conducted in the simultaneously obtained CSF and serum samples of the enrolled patients, with three non-COVID-19 patients with matched demographic features used as the controls for proteomic analysis.
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