Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Host transcriptome response to SARS-CoV2 infection

ABSTRACT: HEK293T stable express hACE2 was infected by SARS-CoV-2 (WA1) and RNA-seq was performed to profile host gene expression in response to SARS-COV-2 infection

ORGANISM(S): Homo sapiens

PROVIDER: GSE169158 | GEO | 2021/04/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Viral and Host Small RNA Response to SARS-CoV-2 Infection

Project description:HEK293T cells overexpressing hACE2 were infected by SARS-CoV-2 (WA1) and small RNA-seq was performed to profile small RNAs in response to SARS-COV-2 infection

2022-10-08 | GSE189920 | GEO

RNA-Seq Quantitative Analysis of the regulation of SARS-CoV-2 infection on autophagy and apoptosis related gene transcriptome in infected cells

Project description:In our study, we found that SARS-CoV-2-S pseudovirions infection induced high levels of autophagy and apoptosis in infected cells. To further investigate the underlying regualtion of SARS-CoV-2-S pseudovirions infection in infected cells, ACE2-expressing HEK293T-hACE2 and Vero E6 cells were treated with Mock or SARS-CoV-2-S pseudovirions for RNA-Seq analysis to exame the expression of autophagy- and apoptosis-related genes. Our results indicate that the majority of autophagy- and apoptosis-promoting genes were significantly increased in SARS-CoV-2-S pseudovirions treated HEK293T-hACE2 and Vero E6 cells. In contrast, the subset of autophagy- and apoptosis-suppressing genes was significantly decreased in SARS-CoV-2-S pseudovirions-treated HEK293T-hACE2 and Vero E6 cells than Mock-treated HEK293T-hACE2 and Vero E6 cells. Meanwhile, SARS-CoV-2-S pseudovirions infection enhanced the expression of pro-inflammatory cytokines in infected cells.

2021-03-23 | GSE169370 | GEO

A Single Intranasal Vaccination with a Rationally Attenuated SARS-CoV-2 Elicits Strong Humoral Immune Response and Is Protective in Syrian Hamsters

Project description:Very few live attenuated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines are currently in pre-clinical or clinical development. We rationally attenuated SARS-CoV-2 (isolate WA1/2020) by removing the polybasic cleavage site within the spike protein and the open reading frames (ORFs) 6-8, and by introducing a pair of mutations into the non-structural protein 1 (Nsp1). The derived virus (WA1-DPRRA-ORF6-8-Nsp1K164A/H165A) became severely attenuated in both the K18-human ACE2 (hACE2) transgenic mice and in Syrian hamsters. Transcriptomic profiling of nasal turbinates and lung tissues of infected Syrian hamsters confirmed that WA1-DPRRA-ORF6-8-Nsp1K164A/H165A attenuated the upregulation of proinflammatory pathways. A single intranasal immunization of just 100 PFU of the WA1-DPRRA-ORF6-8-Nsp1K164A/H165A elicited binding and neutralizing antibody responses in Syrian hamsters and completely protected against SARS-CoV-2-induced weight loss and pneumonia. These data demonstrate the feasibility of rational attenuation of SARS-CoV-2. WA1-DPRRA-ORF6-8-Nsp1K164A/H165A represents a promising live attenuated vaccine candidate.

2022-04-04 | GSE199922 | GEO

Responses to SARS-CoV-2 variants in hACE2 transgenic mice

Project description:hACE2 transgenic mice were infected with the original SARS-CoV-2 strain (B.1) and the Beta (B.1.351) variant. Lung and spleen samples were collected 1 day post infection (DPI), 3 DPI and 5 DPI, and mRNA was sequenced.

2023-09-22 | E-MTAB-13308 | biostudies-arrayexpress

Modelling SARS-CoV-2 Infection in Mice Using Lentiviral hACE2 Vectors Suggests Two Modes of Immune Responses to SARS-CoV-2 Infection

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected millions of individuals worldwide, causing a severe global pandemic. Mice models are wildly used to investigate viral infection pathology, antiviral drugs, and vaccine development. However, since wild-type mice do not express human angiotensin-converting enzyme 2 (hACE2), which mediates SARS-CoV-2 entry into human cells, they are not susceptible to infection with SARS-CoV-2 and are not suitable to simulate symptomatic COVID-19 disease. HACE2 transgenic mice could provide an efficient model, but they are expensive, not always readily available and practically restricted to specific strain(s). Since additional models are needed to study the disease at varying genetic and immune backgrounds, there is a dearth of mouse models for SARS-CoV-2 infection. Here we report the application of lentiviral vectors to generate hACE2 expression in mouse lung epithelial cells (LET1) as well as in interferon receptor knock-out (IFNAR1-/-) mice. Lenti-hACE2 transduction supported SARS-CoV-2 replication both in vitro and in vivo, simulating mild acute lung disease1. Gene expression analysis revealed two modes of immune responses to SARS-CoV-2 infection: one in response to the exposure of mouse lungs to SARS-CoV-2 particles in the absence of productive viral replication, and the second in response to a productive infection. This approach expands our knowledge on the role of type-1 interferon signaling in COVID-19 disease, and can be further implemented for a range of COVID-19 studies and drug development.

2021-12-07 | GSE186167 | GEO

SARS-CoV-2 stock sequencing for infection of nonhuman primates

Project description:SARS-CoV-2 USA/WA1 strain stock was sequenced to determine whether the furin cleavage site was intact.

2020-11-28 | GSE162247 | GEO

Upper respiratory infection drives clinical signs and inflammatory responses in heterologous challenge of SARS-CoV-2 variants of concern

Project description:During the COVID-19 pandemic, three variants of concern (VOC) of the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) emerged globally with increasingly greater ability to evade the immune response and enhanced transmissibility. A critical question we have faced with each new VOC is how well the vaccine based on the ancestral strain will protect. Given vaccine hesitancy, it is also important to address how prior live infections may protect against new variants. To address this later question, K18-hACE2 mice were infected with a low, partially lethal dose of WA1/2020 (WA1), the prototype strain on which the mRNA vaccines are based. On 24 days post-infection (dpi), surviving mice were challenged with WA1, Alpha or Delta. Nasal turbinates and lungs showed active replication on 1- and 3-days post-challenge (dpc) in Alpha- and Delta-, but not WA1- challenge groups. The rate of recovery of Alpha- and Delta-challenged mice lagged behind WA1 with mice showing weight loss despite a greatly dampened proinflammatory response in the lung. In contrast, nasal turbinates had a heightened proinflammatory response for Alpha- and Delta- but not WA1-challenged groups. Inflammatory responses were limited to the upper respiratory tract. Despite this, we did not observe significant difference among the groups in fold change in the neutralizing titer. In summary, infection with a low dose of SARS-CoV-2 confers protection from challenge, but mice in the heterologous challenge group differed in having greater weight loss, viral replication, and a heightened proinflammatory response in the upper respiratory tract.

2023-03-01 | GSE216048 | GEO

Effect of SARS-CoV-2 infection on gene expression of iPSC derived sensory neurons [scRNAseq]

2023-08-04 | GSE227529 | 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

Effect of SARS-CoV-2 infection on gene expression of iPSC derived sensory neurons [bulkRNAseq]

Project description:To investigate the impact of SARS-CoV-2 on the peripheral nervous system, we generated human sensory neurons from induced pluripotent stem cells (iPSC) that we further infected with the SARS-CoV-2 strain WA1/2020 for 48 hours. We then performed gene expression profiling analysis using data obtained from RNA-seq of mock treated cells compared to SARS-CoV-2 infected cells.

2023-08-04 | GSE227528 | GEO

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