Ontology highlight
ABSTRACT:
PROVIDER: PRJEB60441 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| mblSNPs2_CAM.vcf.csi | Other | |||
| mblSNPs2_CAM.vcf.gz | Vcf | |||
| mblSNPs2_BUD.vcf.csi | Other | |||
| mblSNPs2_BUD.vcf.gz | Vcf |
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Project description:Complement lectin pathway activation is associated with COVID-19 disease severity, independent of MBL2 genotype subgroups
2023-03-09 | PRJEB60441 | EVA
Project description:Fourteen percent of SARS-CoV-2-infected individuals suffer multi-organ dysfunction and are unable to resume employment for >2 years post-acute COVID-19. Such "long COVID" cases have been linked to SARS-CoV-2 reservoirs and sustained complement activation. We examined the effects of lectin complement pathway MASP2 inhibitor narsoplimab on long COVID patient plasma-driven microvascular endothelial cell (MVEC) injury, comparing results to clinical outcome, plasma proteomics, and MASP2 expression. MASP2 plasma levels were 12.5-fold higher and MASP2 pulmonary deposition greater in long COVID vs. severe acute COVID-19. MVEC were exposed to long COVID plasmas +/- narsoplimab and caspase 8, a marker of cell activation and apoptosis linked to acute COVID-19 pathology, assessed. Narsoplimab suppressed caspase 8 induction. RNAseq identified pathways associated with this activity in long COVID, components of which were reflected by plasma proteomics. Our data, in the context of an early clinical trial in acute COVID-19, recommend exploration of narsoplimab in long COVID-19.
2026-08-17 | GSE343379 | GEO
Project description:COVID-19 induces profound B-cell dysregulation, notably a marked expansion of plasmablasts (PB), whose functional role remains unclear. This study aimed to characterize PB dynamics and functions in COVID-19 and their association with disease severity. We performed longitudinal immune profiling in a prospective cohort of 50 patients with COVID-19 (cohort 1), including flow cytometry-based B-cell immunophenotyping and multiplex cytokine analysis at days 1, 7, 14, and 30. A second retrospective cohort of 282 corticosteroid-naïve patients (cohort 2) was used to validate PB dynamics, model PB trajectories, and perform transcriptomic profiling of sorted PB. PB expansion occurred early in COVID-19 and was positively correlated with maximal disease severity (r=0.53, p<0.0001). Two distinct PB expansion trajectories were identified: one rapidly resolving, and one persistent and amplified, the latter being associated with higher severity scores and 30-day mortality (31% vs. 5%, p<0.001). In cohort 1, BAFF levels at day 7 correlated positively with both PB proportion (r=0.59, p=0.002) and maximal disease severity (r=0.74, p<0.001). Transcriptomic profiling of PB in cohort 2 revealed severity-specific signatures: in severe cases, early PB upregulated genes related to purine metabolism and CD39 expression, suggesting a pro-inflammatory role. In non-severe cases, PB expressed interferon-related and CIITA-mediated MHC-II programs, indicative of antiviral function. PB display dual functional profiles in COVID-19, acting either as regulators of antiviral immunity or as amplifiers of inflammation in severe disease. These findings support exploring therapeutic strategies targeting the BAFF-PB axis in severe COVID-19.
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Project description:Infection with SARS-CoV-2 has highly variable clinical manifestations, ranging from asymptomatic infection through to life-threatening disease. Host whole blood transcriptomics can offer unique insights into the biological processes underpinning infection and disease, as well as severity. We performed whole blood RNA-Sequencing of individuals with varying degrees of COVID-19 severity. We used differential expression analysis and pathway enrichment analysis to explore how the blood transcriptome differs between individuals with mild, moderate, and severe COVID-19, performing pairwise comparisons between groups.
2022-07-19 | E-MTAB-10926 | biostudies-arrayexpress
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Project description:Severe coronavirus disease 2019 (COVID-19) infection may lead to lung injury, multi-organ failure, and eventually death. Cytokine storm due to excess cytokine production has been associated with fatality in severe infections. However, the specific molecular signatures associated with the elevated immune response are yet to be elucidated. We performed a mass-spectrometry-based proteomic and metabolomic analysis of COVID-19 plasma samples collected at two time points. Using Orbitrap Fusion LC-MS/MS-based label-free proteomic analysis, we identified around 10 significant proteins, 32 significant peptides, and 5 metabolites that were dysregulated at the severe time points. Few of these proteins identified by quantitative proteomics were validated using the multiple reaction monitoring (MRM) assay. Integrated pathway analysis using distinct proteomic and metabolomic signatures revealed alterations in complement and coagulation cascade, platelet aggregation, myeloid leukocyte activation pathway, and arginine metabolism. Further, we highlight the role of leukocyte activation and arginine metabolism in COVID-19 pathogenesis and targeting these pathways for COVID-19 therapeutics.
2022-01-18 | MTBLS2469 | MetaboLights
Project description:Complement overactivation, has been verified in COVID-19 patients. Complement regulatory proteins, including CD55, control complement overactivation thus eliminating complement deposition and cell lysis. We investigated complement regulatory protein expression in COVID-19 for potential deregulated expression patterns driving disease pathogenesis. Single-cell RNA-seq revealed increased PBMCs CD55 expression in severely and critically ill patients. This increase was also detected upon integrated subclustering analysis of monocyte, T cell and B cell populations. FACS analysis confirmed the significant upregulation of CD55 expression in CD4+ and CD8+ T cell and monocyte populations of severely and critically ill COVID-19 patients. This upregulation was associated with decreased expression of type-I IFN-stimulated genes (ISGs) in patients with severe and critical COVID-19, indicating a suppressor effect of CD55. Silencing of CD55 in T cells from COVID-19 severely ill patients in-vitro and sensitization with SARS-CoV-2 peptides resulted in significantly augmented expression of ISGs and a reversal of their expression to levels similar to control or higher. The present study uncovers, to the best of our knowledge, a novel regulatory effect of CD55 on type-I IFN responses of severely ill COVID-19 patients, thus indicating its contribution to COVID-19 pathogenesis, and identifies a novel mechanistic pathway in the COVID-19 immune response.
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Project description:Complement overactivation, has been verified in COVID-19 patients. Complement regulatory proteins, including CD55, control complement overactivation thus eliminating complement deposition and cell lysis. We investigated complement regulatory protein expression in COVID-19 for potential deregulated expression patterns driving disease pathogenesis. Single-cell RNA-seq revealed increased PBMCs CD55 expression in severely and critically ill patients. This increase was also detected upon integrated subclustering analysis of monocyte, T cell and B cell populations. FACS analysis confirmed the significant upregulation of CD55 expression in CD4+ and CD8+ T cell and monocyte populations of severely and critically ill COVID-19 patients. This upregulation was associated with decreased expression of type-I IFN-stimulated genes (ISGs) in patients with severe and critical COVID-19, indicating a suppressor effect of CD55. Silencing of CD55 in T cells from COVID-19 severely ill patients in-vitro and sensitization with SARS-CoV-2 peptides resulted in significantly augmented expression of ISGs and a reversal of their expression to levels similar to control or higher. The present study uncovers, to the best of our knowledge, a novel regulatory effect of CD55 on type-I IFN responses of severely ill COVID-19 patients, thus indicating its contribution to COVID-19 pathogenesis, and identifies a novel mechanistic pathway in the COVID-19 immune response.
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Project description:Background: COVID-19 has infected more than 100-million worldwide. Children appear less susceptible to COVID-19 and present with milder symptoms. Cases of children with COVID-19 developing clinical features of Kawasaki-disease have been described. Methods: We utilised SWATH-MS proteomics to determine the plasma proteins expressed in healthy children, children with multisystem inflammatory syndrome (MIS-C) and children with COVID-19 induced ARDS. Pathway analyses were performed to determine the affected pathways. Results: 76 proteins were differentially expressed across the groups, with 85 and 52 proteins specific to MIS-C and COVID-19 ARDS. Complement and coagulation activation were implicated in these clinical phenotypes, however there was contribution of FcGR and BCR activation in MIS-C and scavenging of heme and retinoid metabolism in COVID-19 ARDS. Conclusions: We show proteome differences in MIS-C and COVID-ARDS, although both show complement and coagulation dysregulation. The results may be helpful in developing therapeutic targets that could improve the outcomes for these children.
2022-04-06 | PXD025125 | Pride