Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1056321 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Repeated Omicron infection alleviates SARS-CoV-2 immune imprinting
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Project description:SHAE004: SARS-CoV, SARS-dORF6 and SARS-BatSRBD infection of HAE cultures.
2025-01-24 | E-GEOD-47962 | ExpressionAtlas
Project description:A pivotal role of astrocytes in the pathophysiology of CNS disorders during the SARS-CoV-2 infection of brain has been proposed. Thus, the study was performed to reveal astrocyte response to infection caused by either Omicron or Delta variant.
2025-03-01 | E-MTAB-14745 | biostudies-arrayexpress
Project description:The ancestral SARS-CoV-2 strain that initiated the Covid-19 pandemic at the end of 2019 has rapidly mutated into multiple variants of concern with variable pathogenicity and increasing immune escape strategies. However, differences in host cellular antiviral responses upon infection with SARS-CoV-2 variants remains elusive. Leveraging whole cell proteomics, we determined host signalling pathways that are differentially modulated upon infection with the clinical isolates of the ancestral SARS-CoV-2 B.1 and the variants of concern Delta and Omicron BA.1. Our findings illustrate alterations in the global host proteome landscape upon infection with SARS-CoV-2 variants and the resulting host immune responses. Additionally, viral proteome kinetics reveal declining levels of viral protein expression during Omicron BA.1 infection when compared to ancestral B.1 and Delta variants, consistent with its reduced replication rates. Moreover, molecular assays reveal deferral activation of specific host antiviral signalling upon Omicron BA.1 and BA.2 infection. Our study provides an overview of host proteome profile of multiple SARS-CoV-2 variants and brings forth a better understanding of the instigation of key immune signalling pathways causative for the differential pathogenicity of SARS-CoV-2 variants.
2023-05-10 | PXD037265 | Pride
Project description:Omicron is currently the dominant SARS-CoV-2 variant and several sublineages have emerged. Questions remain about the impact of previous SARS-CoV-2 exposure on cross-variant immune responses elicited by the SARS-CoV-2 Omicron sublineage BA.2 compared to BA.1. Here we show that without previous history of COVID-19, BA.2 infection induces a reduced immune response against all variants of concern (VOC) compared to BA.1 infection. The absence of ACE2 binding in sera of previously naïve BA.1 and BA.2 patients indicates a lack of meaningful neutralization. In contrast, anti-spike antibody levels and neutralizing activity greatly increased in the BA.1 and BA.2 patients with a previous history of COVID-19. Transcriptome analyses of peripheral immune cells showed significant differences in immune response and specific antibody generation between BA.1 and BA.2 patients as well as significant differences in the expression of specific immune genes. In summary, prior infection status significantly impacts the innate and adaptive immune response against VOC following BA.2 infection.
2022-12-20 | GSE205244 | GEO
Project description:A critical aspect of the mechanism of SARS-CoV-2 infection is the protease-mediated activation of the viral spike (S) protein. The type II transmembrane serine protease TMPRSS2 is crucial for SARS-CoV-2 infection in lung epithelial Calu-3 cells and murine airways. However, the importance of TMPRSS2 needs to be re-examined because the ability to utilize TMPRSS2 is significantly reduced in the Omicron variants that spread globally. For this purpose, replication profiles of SARS-CoV-2 were analyzed in human respiratory organoids. All tested viruses, including Omicron variants, replicated efficiently in these organoids. Notably, all SARS-CoV-2 strains retained replication ability in TMPRSS2-gene knockout (KO) respiratory organoids, suggesting that TMPRSS2 is not essential for SARS-CoV-2 infection in human respiratory tissues. However, TMPRSS2-gene knockout significantly reduces the inhibitory effect of nafamostat, suggesting the advantage of TMPRSS2-utilizing ability for the SARS-CoV-2 infection in these organoids. Interestingly, Omicron variants regained the TMPRSS2-utilizing ability in recent subvariants. The basal infectivity would be supported mainly by cathepsins because the cathepsin inhibitor, EST, showed a significant inhibitory effect on infection with any SARS-CoV-2 strains, mainly when used with nafamostat. A supplementary contribution of other serine proteases was also suggested because the infection of the Delta variant was still inhibited partially by nafamostat in TMPRSS2 KO organoids. Thus, various proteases, including TMPRSS2, other serine proteases, and cathepsins, co-operatively contribute to SARS-CoV-2 infection significantly in the respiratory organoids. Thus, SARS-CoV-2 infection in the human respiratory tissues would be more complex than observed in cell lines or mice.
2024-11-20 | GSE279753 | GEO
Project description:Transcriptional response of human lung epithelial cells to SARS-CoV-2 infection
2020-04-17 | E-GEOD-147507 | ExpressionAtlas
Project description:Ancestral SARS coronavirus-2 (SARS-CoV-2) and variants of concern (VOC) caused a global pandemic with a spectrum of disease variation linked to immune dysfunction. The mechanistic underpinnings of variation related to lung epithelium are relatively understudied. Here, we biobanked lung organoids by preserving stem cell function. We optimized viral infection with H1N1 swine flu and next comprehensively characterized epithelial responses to SARS-CoV-2 infection in phenotypically stable lung organoids from twenty different subjects. We discovered Tetraspanin 8 (TSPAN8) as a novel mediator of SARS-CoV-2-infection. TSPAN8 facilitates SARS-CoV-2 infection rates but does not via enhanced ACE-2-mediated entry. In head-to-head comparisons with Ancestral SARS-CoV-2, Delta- and Omicron- VOC displayed lower overall infection rates of organoids but triggered increased epithelial interferon responses. All variants shared highest tropism for ciliated- and goblet- cells. ACE2- and TSPAN8- expression are universal features of infected cells. TSPAN8-blocking antibodies diminish SARS-CoV-2 infection and may spur novel avenues for COVID-19 therapy.
2022-09-30 | GSE211562 | GEO
Project description:RNA-seq of SARS-CoV-2 infected lungs from mice sensitized for SARS-CoV-2 infection by Ad5-hACE2 transduction compared to non-sensitized mice
2021-03-22 | E-GEOD-150847 | ExpressionAtlas
Project description:A recombinant SARS-CoV lacking the envelope (E) protein is attenuated in vivo. Here we report that E protein PDZ-binding motif (PBM), a domain involved in protein-protein interactions, is a major virulence determinant in vivo. Elimination of SARS-CoV E protein PBM by using reverse genetics led to attenuated viruses (SARS-CoV-mutPBM) and to a reduction in the deleterious exacerbate immune response triggered during infection with the parental virus (SARS-CoV-wt). Cellular protein syntenin bound E protein PBM during SARS-CoV infection. Syntenin activates p38 MAPK leading to overexpression of inflammatory cytokines, and we have shown that active p38 MAPK was reduced in lungs of mice infected with SARS-CoVs lacking E protein PBM (SARS-CoV-mutPBM) as compared with the parental virus (SARS-CoV-wt), leading to a decreased expression of inflammatory cytokines and to viral attenuation. Therefore, E protein PBM is a virulence factor that activates pathogenic immune response most likely by using syntenin as a mediator of p38 MAPK induced inflammation. Three biological replicates were independently hybridized (one channel per slide) for each sample type (SARS-CoV-wt, SARS-CoV-mutPBM, Mock). Slides were Sure Print G3 Agilent 8x60K Mouse (G4852A-028005)
2014-10-31 | E-GEOD-52920 | biostudies-arrayexpress