Similar Datasets
Project description:This study addresses the question how host cells transcriptionally respond to SARS-CoV2 infection.
2023-12-02 | GSE162492 | GEO
Project description:This study addresses the question how host cells transcriptionally respond to SARS-CoV2 infection.
2023-12-02 | GSE162494 | GEO
Project description:This dataset looks at the transcriptome of in vitro-differentiated primary lung cells infected with SARS-CoV2. Some cells have been treated with the drug Enzalutamide.
2022-05-04 | E-MTAB-10687 | biostudies-arrayexpress
Project description:RNA-Seq was carried out in order to obtain the time dependent expression dynamics of SARS-CoV2 (Trondheim strain)-induced transcriptome changes in human lung epithelial Calu-3 cells.
2022-10-25 | E-MTAB-12134 | biostudies-arrayexpress
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
Project description:This dataset looks at the transcriptome of in vitro-differentiated primary lung cells during an infection time course of SARS-CoV2. Some cells have been treated with the drug Enzalutamide. Cells from one man and one female were mixed to minimize the technical variability, and can be separated by SNPs (SNPs not included, but the calculated cell-donor associations are provided).
2023-04-01 | E-MTAB-10697 | biostudies-arrayexpress
Project description:RNAseq analysis of human immune cells (monocytes CD14+ and B cells CD19+) cocultured with SARS-CoV2, influenza A or Ebola viruses-infected epithelial cells as well as directly infected or SARS-CoV2 single protein transfected epithelial cells
2021-10-29 | GSE186650 | GEO
Project description:Pathogenic mechanisms underlying severe SARS-CoV2 infection remain largely unelucidated. High-throughput sequencing technologies that capture genome and transcriptome information are key approaches to gain detailed mechanistic insights from infected cells. These techniques readily detect both pathogen and host-derived sequences, providing a means of studying host-pathogen interactions. Recent studies have reported the presence of host-virus chimeric (HVC) RNA in RNA-seq data from SARS-CoV2 infected cells and interpreted these findings as evidence of viral integration in the human genome as a pathogenic mechanism. Since SARS-CoV2 is a positive sense RNA virus that replicates in the cytoplasm it does not have a nuclear phase in its life cycle, so it is biologically unlikely to be in a location where splicing events could result in genome integration. Here, we investigated the biological authenticity of HVC events. In contrast to true biological events, e.g. mRNA splicing and genome rearrangement events, which generate reproducible chimeric sequencing fragments across different biological isolates, we found that HVC events across >100 RNA-seq libraries from patients with COVID-19 and SARS-CoV2 infected cell lines, were highly irreproducible. RNA-seq library preparation is inherently error-prone due to random template switching during reverse transcription of RNA to cDNA. By counting chimeric events observed when constructing an RNA-seq library from human RNA and spike-in RNA from an unrelated species, such as fruit-fly, we estimated that ~1% of RNA-seq reads are artifactually chimeric. In SARS-CoV2 RNA-seq we found that the frequency of HVC events were, in fact, no more frequent than this background “noise”. Finally, we developed a novel experimental approach to enrich SARS-CoV2 sequences from bulk RNA of infected cells. This method enriched viral sequences but did not enrich for HVC events, suggesting that the majority of HVC events are, in all likelihood, artifacts of library construction. In conclusion, our findings indicate that HVC events observed in RNA-sequencing libraries from SARS-CoV2 infected cells are extremely rare and are likely artifacts arising from either random template switching of reverse-transcriptase and/or sequence alignment errors. Therefore, the observed HVC events do not support SARS-CoV2 fusion to cellular genes and/or integration into human genomes.
2021-02-19 | GSE167131 | GEO
Project description:The Angiotensin-converting enzyme 2 (ACE2) receptor is the central entry point for SARS-Cov2. Several SAR-Cov2 substrains have developed mutations in their spike protein to maximize their use of ACE2, e.g. to strengthen ACE2 binding for increased uptake or adapt to specific amino acid properties of ACE2 to cross the species barrier. But little is known about the effect of host regulators on ACE2 and subsequently their impact on SARS-Cov2 infection. Here we identify the E3 ligase MDM2 as a ACE2 modulator. The knockout of MDM2 induced a strong pro-viral effect specific for SARS-Cov2 and we could see the increase of ACE2 levels. This effect is likely dependent on the ubiquitination site Lysine 788, which MDM2 uses to induce proteasomal degradation of ACE2. Substituting this amino acid led to increased ACE2 levels and increased SARS-CoV2 infection facilitated by enhanced SARS-Cov2 uptake.
2023-09-08 | PXD040891 | Pride
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