Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection

ABSTRACT: The antiviral immune response to SARS-CoV-2 infection can limit viral spread and prevent development of pneumonic COVID-19. However, the protective immunological response associated with successful viral containment in the upper airways remain unclear. Here, we combine a multiomics approach with longitudinal sampling to reveal temporally resolved protective immune signatures in non-pneumonic and ambulatory SARS-CoV-2 infected patients and associate specific immune trajectories with upper airway viral containment. We see a distinct systemic rather than local immune state associated with viral containment, characterized by interferon stimulated gene (ISG) upregulation across circulating immune cell subsets in non-pneumonic SARS-CoV2 infection. We report reduced cytotoxic potential of Natural Killer (NK) and T cells, and an immune-modulatory monocyte phenotype with protective immunity in COVID-19. Together, we show protective immune trajectories in SARS-CoV2 infection, which have important implications for patient prognosis and the development of immunomodulatory therapies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193708 | GEO | 2022/01/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection

Project description:The antiviral immune response to SARS-CoV-2 infection can limit viral spread and prevent development of pneumonic COVID-19. However, the protective immunological response associated with successful viral containment in the upper airways remain unclear. Here, we combine a multiomics approach with longitudinal sampling to reveal temporally resolved protective immune signatures in non-pneumonic and ambulatory SARS-CoV-2 infected patients and associate specific immune trajectories with upper airway viral containment. We see a distinct systemic rather than local immune state associated with viral containment, characterized by interferon stimulated gene (ISG) upregulation across circulating immune cell subsets in non-pneumonic SARS-CoV2 infection. We report reduced cytotoxic potential of Natural Killer (NK) and T cells, and an immune-modulatory monocyte phenotype with protective immunity in COVID-19. Together, we show protective immune trajectories in SARS-CoV2 infection, which have important implications for patient prognosis and the development of immunomodulatory therapies.

2022-01-17 | PXD030785 | Pride

Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection

Project description:Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection

| PRJNA797377 | ENA

Ad26.COV2.S Prevents SARS-CoV-2 Induced Pathways of Inflammation and Thrombosis in Hamsters

Project description:Syrian golden hamsters exhibit features of severe disease after SARS-CoV-2 challenge and are therefore useful models of COVID-19 pathogenesis and prevention with vaccines. Recent studies have shown that SARS-CoV-2 infection stimulates type I interferon, myeloid, and inflammatory signatures similar to human disease, and that weight loss can be prevented with vaccines. However, the impact of vaccination on transcriptional programs associated with COVID-19 pathogenesis and protective adaptive immune responses is unknown. Here we show that SARS-CoV-2 challenge in hamsters stimulates myeloid and inflammatory programs as well as signatures of complement and thrombosis associated with human COVID-19. Notably, single-dose immunization with Ad26.COV2.S, an adenovirus serotype 26 vector (Ad26)-based vaccine expressing a stabilized SARS-CoV-2 spike protein, prevents the upregulation of these pathways such that the gene expression profiles of vaccinated hamsters are comparable to uninfected animals. Furthermore, we validated the protective efficacy of the Ad26.COV2.S against proinflammatory pathways and coagulation cascade in rhesus macaques by proteomics. Finally, we show that Ad26.COV2.S vaccination induces T and B cell signatures that correlate with binding and neutralizing antibody responses. These data provide further insights into the mechanisms of Ad26.COV2.S based protection against severe COVID-19 in hamsters.

2022-03-26 | GSE196893 | GEO

TCR profiling of COVID convalescent and healthy donor whole blood with nCounter

Project description:This study investigated the cellular immune response in people who had recovered from SARS-CoV2 infection(COVID-19).

2022-08-21 | GSE211394 | GEO

Whole Blood profiling of COVID convalescent and Healthy donors with nCounter

Project description:This study investigated the cellular immune response in people who had recovered from SARS-CoV2 infection (COVID-19).

2022-08-21 | GSE211378 | GEO

SARS-CoV-2 produces a microRNA, CoV2-miR-O8, in patients with COVID-19 infection

Project description:SARS-CoV-2 can generate viral microRNAs (v-miRNAs) that target host gene expression. This study used small RNAseq to identify the v-miRNAs present in COVID-19 patients' nasopharyngeal swabs. The study identified a specific conserved v-miRNA sequence (CoV2-miR-O8) unique to SARS-CoV-2 that is highly present in COVID-19 patients' samples, interacts with Argonaute, and has features consistent with Dicer and Drosha generation. CoV2-miR-O8 is predicted to target specific human genes and can be detected by RTPCR assays in patients.

2023-12-11 | GSE230080 | GEO

Functional Assessment of US SARS-CoV-2 L452R Epsilon Variant

Project description:The multiple mutations comprising the epsilon variant demonstrates the independent convergent evolution of SARS-CoV-2 with its spike protein mutation L452R also present in the delta variant. Cells infected with live viral samples of the epsilon viral variant compared to non-epsilon variant displayed increased sensitivity to neutralization antibodies (NAb) suggesting an intact humoral response (P< 1.0 e-4). The ability for SARS-CoV2 to become more infectious but less virulent is supported mechanistically in the downregulation of viral processing pathways seen by multiomic analyses. Importantly, this paired transcriptomics and proteomic profiling of cellular response to live virus revealed an altered leukocyte response and metabolic mRNA processing in cells upon live viral infection of the epsilon variant. To ascertain host response to SARS-CoV-2 infection, primary COVID-19 positive nasopharyngeal samples were transcriptomically profiled a differential innate immune response (P<2.0 e-12) but, a relatively unaltered T cell response in the patients carrying the epsilon variant (P< 2.0 e-3). In fact, patients infected with SARS-CoV-2 and those vaccinated with the BNT162b2 vaccine have comparable CD4+/CD8+ T-cell immune responses to the B.1.429 variant (P<5 e-2). The epsilon variant alters viral processing response in infected cells, and the host innate immune response in COVID-19 positive nasopharyngeal swabs, but generates a protective host T cell response molecular signature in both vaccinated and unvaccinated patients.

2022-05-06 | PXD027995 | Pride

Evasion of antiviral innate immunity by SARS-CoV-2 NSP1 is exerted through H3K9 di-methylation

Project description:The pathogen causing the current COVID-19 pandemic, the severe acute respiratory syndrome coronavirus (SARS-CoV-2), evades the innate immune machinery through the independent action of several viral proteins, including the nonstructural protein 1 (NSP1). NSP1 has multiple functions, but the relative contribution of NSP1-mediated translational repression, ribosome-proximate degradation of host mRNA, or other molecular mechanisms to viral immune evasion remains unclear. Here we combined several genome wide approaches, including RNA-seq, ribosome footprinting, and ChIP-seq to find that NSP1 predominantly affects transcription of immune-related genes. NSP1 expression in A549 cells induced Histone 3 Lysine 9 (H3K9) methylation of antiviral gene loci, leading to specific suppression of type I and type III interferon pathways. Treatment with the G9a/GLP H3K9 methyltransferase inhibitor UNC0638 reverses this suppression of antiviral genes and blocks viral replication after SARS-CoV2 infection of A549 cells. Our results call attention to epigenetic reprogramming induced by SARS-CoV2 and highlight the importance to identify innate factors regulating histone modification of gene loci targeted by SARS-CoV-2, with possible relevance to the understanding and therapy of other immunomodulatory diseases.

2023-07-12 | GSE208116 | GEO

IL-9 exacerbates SARS-CoV2 infection and associated airway inflammation

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus diseases 2019 (COVID-19) and broncho-alveolar inflammation (Merad and Martin, 2020). IL-9 induces airway inflammation and bronchial hyper responsiveness in respiratory viral illnesses and allergic inflammation (Temann et al., 1998). However, the role of IL-9 is not yet identified in SARS-CoV2 infection. Here we show that IL-9 promotes SARS-CoV2 infection and airway inflammation in K18-hACE2 transgenic (ACE2.Tg) mice, as IL-9 blockade reduces SARS-CoV2 infection and suppressed airway inflammation. Foxo1 is essential for the induction of IL-9 in helper T (Th) cells (Malik et al., 2017). While ACE2.Tg mice with Foxo1-deficiency in CD4+ T cells were performed to be resistant to SARS-CoV2 infection associated with reduced IL-9 production, exogenous IL-9 made Foxo1-deficient mice susceptible to SARS-CoV2 infection with increased airway inflammation. Collectively, we identify a mechanistic insight of IL-9-mediated regulation of antiviral and inflammatory pathways in SARS-CoV2 infection, and unravel a principle for the development of host-directed therapeutics to mitigate disease severity.

2022-07-22 | GSE209550 | GEO

Analysis of blood and nasal epithelial transcriptomes to identify mechanisms associated with control of SARS-CoV-2 viral load in the upper respiratory tract

Project description:The amount of SARS-CoV-2 detected in the upper respiratory tract (URT viral load) is a key driver of transmission of infection. Current evidence suggests that mechanisms constraining URT viral load are different from those controlling lower respiratory tract viral load and disease severity. Understanding such mechanisms may help to develop treatments and vaccine strategies to reduce transmission. Combining mathematical modelling of URT viral load dynamics with transcriptome analyses we aimed to identify mechanisms controlling URT viral load. COVID-19 patients were recruited in Spain during the first wave of the pandemic. RNA sequencing of peripheral blood and targeted NanoString nCounter transcriptome analysis of nasal epithelium were performed and gene expression analysed in relation to paired URT viral load samples collected within 15 days of symptom onset. Proportions of major immune cells in blood were estimated from transcriptional data using computational differential estimation. Weighted correlation network analysis (adjusted for cell proportions) and fixed transcriptional repertoire analysis were used to identify associations with URT viral load, quantified as standard deviations (z-scores) from an expected trajectory over time.

2023-04-01 | E-MTAB-12791 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data