Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of SIRT5-KO cells infected with SARS-CoV-2

ABSTRACT: We are studying the role of human sirtuin SIRT5 during viral infection with SARS-CoV-2. We performed RNA-sequencing of WT and SIRT5-KO human lung adenocarinoma A549 cells overexpressing ACE2 (A549-ACE2), in infected and mock-infected conditions. . Our analysis revealed that SARS-CoV-2 replication is attenuated in SIRT5-KO cells. In addition, SIRT5-KO cells expressed higher basal levels of innate immunity markers and mounted a stronger antiviral response. Our results indicate that SIRT5 is a proviral factor necessary for efficient viral replication.

ORGANISM(S): Homo sapiens

PROVIDER: GSE188382 | GEO | 2021/11/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

In vivo inhibition of nuclear ACE2 translocation protects against SARS-CoV-2 replication and lung damage through epigenetic imprinting

Project description:In vitro, ACE2 translocates to the nucleus to induce SARS-CoV-2 replication. Here, using digital spatial profiling of lung tissues from SARS-CoV-2-infected golden Syrian hamsters, we show that a specific and selective peptide inhibitor of nuclear ACE2 (NACE2i) inhibits viral replication two days after SARS-CoV-2 infection. NACE2i also prevents inflammation and macrophage infiltration, and increases NK cell infiltration in bronchioles. NACE2i treatment restores host translation in infected hamster bronchiolar cells.

2023-06-01 | GSE233642 | GEO

SARS-CoV-2 infected and uninfected VeroE6 and A549-ACE2: Bemcentinib and liposome treatments

Project description:VeroE6 or A549-ACE2 cells were treated with inhibitors of phosphatidylserine receptors and infected with SARS-CoV-2.

2021-06-26 | GSE178942 | GEO

Identification of required host factors for SARS-CoV-2 infection in human cells [RNA-seq]

Project description:RNA-seq was performed to determine gene expression (RNA) levels and SARS-CoV-2 viral reads in A549-ACE2 cells treated with DMSO or Amlodipine.

2020-10-24 | GSE159522 | GEO

SIRT5 is a proviral factor that interacts with SARS-CoV-2 Nsp14 protein

Project description:SARS-CoV-2 non-structural protein Nsp14 is a highly conserved enzyme necessary for viral replication. Nsp14 forms a stable complex with non-structural protein Nsp10 and exhibits exoribonuclease and N7-methyltransferase activities. Protein-interactome studies identified human sirtuin 5 (SIRT5) as a putative binding partner of Nsp14. SIRT5 is an NAD-dependent protein deacylase critical for cellular metabolism that removes succinyl and malonyl groups from lysine residues. Here we investigated the nature of this interaction and the role of SIRT5 during SARS-CoV-2 infection. We showed that SIRT5 stably interacts with Nsp14, but not with Nsp10, suggesting that SIRT5 and Nsp10 are parts of separate complexes. We found that SIRT5 catalytic domain is necessary for the interaction with Nsp14, but that Nsp14 does not appear to be directly deacylated by SIRT5. Furthermore, knock-out of SIRT5 or treatment with specific SIRT5 inhibitors reduced SARS-CoV-2 viral levels in cell-culture experiments. SIRT5 knock-out cells expressed higher basal levels of innate immunity markers and mounted a stronger antiviral response. Our results indicate that SIRT5 is a proviral factor necessary for efficient viral replication, which opens novel avenues for therapeutic interventions.

2021-12-19 | MSV000088589 | MassIVE

Nanobodies agains Sars Cov 2 Nsp9 protein protects cells from virus infection

Project description:Nanobodies are emerging as ideal instruments for drug design and several have recently been created to block SARS-Cov-2 entry in the host cell by targeting surface-exposed Spike protein. However, due to the high frequency of mutations that affect Spike, these nanobodies may not efficiently target Spike during viral entry. Here we have established a pipeline that instead targets highly conserved viral proteins that are made only after viral entry into the host cell when the SARS-Cov-2 RNA-based genome is translated. As proof of principle, we designed nanobodies against the SARS-CoV-2 non-structural protein Nsp9, required for replication of the viral genome. To find out if this strategy efficiently blocked viral replication, one of these anti-Nsp9 nanobodies, 2NSP23, previously characterized using immunoassays and NMR spectroscopy for epitope mapping, was encapsulated into lipid nanoparticles (LNP) as mRNA. We show that this nanobody, hereby referred to as LNP-mRNA-2NSP23, is internalized and translated in HEK293 cells. We next infected HEK293-ACE2 cells subjected to LNP-mRNA-2NSP23 with multiple SARS-CoV-2 variants. Analysis of total RNA isolated form infected cells treated or untreated with LNP-mRNA-2NSP23 using qPCR and RNA deep sequencing shows that the LNP-mRNA-2NSP23 nanobody protects HEK293-ACE2 cells and suppresses replication of several SARS-CoV-2 variants. These observations indicate that following translation, the nanobody 2NSP23 inhibits viral replication by targeting Nsp9 in living cells. We propose that LNP-mRNA-2NSP23 may be translated into an innovative technology to generate novel antiviral drugs highly efficient across coronaviruses.

2023-10-10 | GSE244714 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Mock/SARS-CoV-2 Infected humanized ACE2 Mice Olfactory Epithelium and Olfactory Bulb Transcriptomes

Project description:SARS-CoV-2 infection causes a wide spectrum of clinical manifestations in human, and olfactory dysfunction represents as one of the most predictive and common symptoms in COVID-19 patients. Herein we demonstrate intranasal inoculation of SARS-CoV-2 induces robust viral replication in the olfactory epithelium (OE), not olfactory bulb (OB), resulting in transient olfactory dysfunction in humanized ACE2 mice. To decipher the underlying mechanism of the observed olfactory dysfunction in SARS-CoV-2 infected mice at the molecular level, RNA-Seq analyses of the OE and OB samples from SARS-CoV-2 infected mice were performed in comparison with that from the control animals.

2021-07-12 | GSE173186 | GEO

ORAI1 establishes resistance to SARS-CoV-2 infection by regulating tonic type I interferon levels

Project description:We report RNAseq analysis of control, ORAI1KO and STIM1 KO (knockout) HEK293-ACE2 cells under uninfected (mock) and SARS-CoV-2-infected conditions

2021-05-20 | GSE173707 | GEO

C4PR_LIV: N-terminomic analysis of SARS-CoV-2-infected ACE2-A549 cells (Unenriched)

Project description:Many events in viral infection are regulated through post-translational modification. In the case of positive-sense RNA viruses such as SARS-CoV-2 which encodes two viral proteases, proteolytic cleavage of both viral and cellular proteins is crucial for productive viral infection. In this work we study proteolysis in the context of SARS-CoV-2 infection of ACE2-A549 and Vero E6 cells, infected at a multiplicity of infection of 1, with samples harvested at 0,6,12 and 24h post-infection. Neo-N-termini and lysine residues were labelled at the protein level with TMTpro reagents prior to tryptic digestion. For unenriched samples, the trypsin-digested material was then fractionated offline, and analysed by LC-MS/MS for the study of total protein abundance over the infection timecourse. For enriched samples, unblocked neo-N-termini generated by tryptic digested were labelled with undecanal and depleted, yielding a sample enriched for blocked neo-N-termini (TMTpro, N-terminal acetylation, and pyroGlu). The enriched samples were similarly fractionated offline and analysed by LC-MS/MS. Please note this is one of several linked datasets. This dataset contains data from ACE2-A549 cells infected with SARS-CoV-2, prior to enrichment.

2021-07-29 | PXD021145 | Pride

Modeling SARS-CoV-2 infection and its individual differences with ACE2-expressing human iPS cells

Project description:Genetic differences are a primary reason for differences in the susceptibility and severity of COVID-19. As induced pluripotent stem (iPS) cells maintain the genetic information of the donor, they can be used to model individual differences in SARS-CoV-2 infection in vitro. We found that human iPS cells expressing the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) (ACE2-iPS cells) can be infected w SARS-CoV-2. In infected ACE2-iPS cells, the expression of SARS-CoV-2 nucleocapsid protein, budding of viral particles, and production of progeny virus, double membrane spherules, and double-membrane vesicles were confirmed. We performed SARS-CoV-2 infection experiments on ACE2-iPS/ embryonic stem (ES) cells from eight individuals. Male iPS/ES cells were more capable of producing the virus compared with female iPS/ES cells. These findings suggest that ACE2-iPS cells can not only reproduce individual differences in SARS-CoV-2 infection in vitro but also are a useful resource to clarify the causes of individual differences in COVID-19 due to genetic differences.

2021-04-18 | GSE166990 | GEO

RNAseq analyses in HEK293T-ACE2 cells infected with SARS-CoV-2 (VOC Delta, 24hours) vs untreated cells

Project description:In this study a gene expression (i.e., RNAseq) analysis was performed in HEK293T-ACE2 cellular model upon infection with viral particle belonging to VOC Delta (MOI: 0.026) for 24 hours in order to have a global picture of the transcriptome landscape in response to early phase of infection of SARS-CoV-2 ( VOC Delta infection and to evaluate the role of Ca2+ in HEK293-ACE2 cellular model and transfer to homeostasis in SARS-COV-2 patients (by Pasqualino de Antonellis1-2* and Veronica Ferrucci 1-2* (first authors) et al. and Massimo Zollo1-2# (corresponding author). Manuscript in preparation 2022 July 15th 2022. Short title "ATP2B1 (PMCA1), regulated by FOXO3, influences susceptibility to severe COVID19".

2022-12-01 | E-MTAB-11973 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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