SARS coronavirus series
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens Viruses
PROVIDER: GSE546 | GEO | 2003/10/19
SECONDARY ACCESSION(S): PRJNA85299
REPOSITORIES: GEO
Similar Datasets
Project description:Set of microarray experiments used to identify an unknown coronavirus in a viral culture derived from a patient with SARS. March 2003. Keywords = SARS Keywords = coronavirus Keywords = viral discovery Keywords = viruses Keywords = respiratory infection
2010-06-05 | E-GEOD-546 | biostudies-arrayexpress
Project description:Differential expression was determined in Calu-3 cells between mock infected and infection with either Human coronavirus EMC and SARS coronavirus at different times post infection. Calu-3 2B4 cells were infected with Human Coronavirus EMC 2012 (HCoV-EMC) or mock infected. Samples were collected 0, 3, 7, 12, 18 and 24 hpi. There are 3 mock and 3 infected replicates for each time point, except for 12 hpi for which there are only 2 infected replicates (one replicate did not pass RNA quality check). There were no mock sampes at 18 hpi, and therefore infected samples at 18 hpi were compared with mocks at 24 hpi. For direct comparison with SARS-CoV infected cells, raw data from HCoV-EMC experiments were quantile normalized together with the SARS-CoV dataset (GEO Series accession number GSE33267).
2013-05-03 | E-GEOD-45042 | biostudies-arrayexpress
Project description:Severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) are zoonotic pathogens that can cause severe respiratory disease in humans. Identification of the host factors that are necessary for viral infection and virus-induced cell death is critical to our understanding of the viral life cycle and can potentially aid the development of new treatment options. Here, we report CRISPR screen results of both SARS-CoV and MERS-CoV infections in derivatives of the human hepatoma cell line Huh7. Our screens identified the known entry receptors ACE2 for SARS-CoV and DPP4 for MERS-CoV. Additionally, the SARS-CoV screen uncovered several components of the NF-κB signaling pathway (CARD10, BCL10, MALT1, MAP3K7, IKBKG), while the MERS-CoV screen revealed the polypyrimidine tract-binding protein PTBP1, the ER scramblase TMEM41B, furin protease and several transcriptional and chromatin regulators as candidate factors for viral replication and/or virus-induced cell death. Together, we present several known and unknown coronavirus host factors that are of interest for further investigation.
2024-01-08 | GSE252396 | GEO
Project description:Abstract: The COVID-19 (Coronavirus disease-2019) pandemic, caused by the SARS-CoV-2 coronavirus, has highlighted emergent viruses as significant threats to public health and the global economy. SARS-CoV-2 is closely related to the more lethal but less transmissible coronaviruses SARS-CoV-1 and MERS-CoV. Here, we have carried out comparative viral-human protein-protein interaction and viral protein localization analysis for all three viruses. We find that proteins often do not change localization across viruses but their sequence divergence dictates differences in host interactions. Functional genetic screening identified host factors that functionally impinge on coronavirus proliferation, including Tom70, a mitochondrial chaperone protein that interacts with both SARS-CoV-1 and SARS-CoV-2 Orf9b, an interaction we structurally characterized using cryoEM. Combining genetically validated host factors with both COVID-19 patient genetic data and medical billing records identified important molecular mechanisms (IL-17 regulation) and drug treatments (sigma-1 receptor ligands) that merit further molecular and clinical study.
2020-10-16 | PXD021588 | Pride
Project description:The COVID-19 pandemic has claimed the lives of more than one million people worldwide. The causative agent, SARS-CoV-2, is a member of the Coronaviridae family, which are viruses that cause respiratory infections of varying severity. The cellular host factors and pathways co-opted by SARS- CoV-2 and other coronaviruses in the execution of their life cycles remain ill-defined. To develop an extensive compendium of host factors required for infection by SARS-CoV-2 and three seasonal coronaviruses (HCoV-OC43, HCoV-NL63, and HCoV-229E), we performed parallel genome-scale CRISPR knockout screens. These screens uncovered multiple host factors and pathways with pan- coronavirus and virus-specific functional roles, including major dependency on glycosaminoglycan biosynthesis, SREBP signaling, BMP signaling, and glycosylphosphatidylinositol biosynthesis, as well as a requirement for several poorly characterized proteins. We identified an absolute requirement for the VTT-domain containing protein TMEM41B for infection by SARS-CoV-2 and three seasonal coronaviruses. This human Coronaviridae host factor compendium represents a rich resource to develop new therapeutic strategies for acute COVID-19 and potential future coronavirus spillover events.
2020-11-24 | GSE162038 | GEO
Project description:We performed genome-wide CRISPR KO screens in human Huh7.5.1 cells to select for mutations that render host cells resistant to viral infection by SARS-CoV-2, human coronavirus 229E and OC43.
2020-10-16 | E-MTAB-9638 | biostudies-arrayexpress
Project description:Differential expression was determined in Calu-3 cells between mock infected and infection with either Human coronavirus EMC and SARS coronavirus at different times post infection.
2013-05-03 | GSE45042 | GEO
Project description:COVID-19 is the third outbreak of zoonotic coronavirus (CoV) of the century after the epidemic Severe acute respiratory syndrome CoV (SARS-CoV) in 2003 and Middle East respiratory syndrome CoV (MERS-CoV) in 2012. Treatment options for CoVs are largely lacking. Here, we show that clofazimine, an anti-leprosy drug with favorable safety and pharmacokinetics profile, possesses pan-coronaviral inhibitory activity, and can antagonize SARS-CoV-2 replication in multiple in vitro systems, including the human embryonic stem cell-derived cardiomyocytes and ex vivo lung cultures. The FDA-approved molecule was found to inhibit multiple steps of viral replication, suggesting polypharmacology is likely underlying its antiviral activity. In a hamster model of SARS-CoV-2 pathogenesis, prophylactic and therapeutic administration of clofazimine significantly reduced lung viral load and fecal viral shedding, as well as reversal of cytokine storm. Additionally, clofazimine exhibited antiviral drug synergy when administered with remdesivir. Since clofazimine is orally bioavailable and has a comparatively low manufacturing cost, it is an attractive clinical candidate for outpatient treatment and remdesivir-based combinatorial therapy for hospitalized COVID-19 patients, particularly in developing countries. Taken together, our data provide evidence that clofazimine may prove effective against current pandemic SARS-CoV-2, endemic MERS-CoV in the Middle East, and, possibly most importantly, emerging CoV of the future.
2021-02-02 | GSE162899 | GEO
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent responsible for the ongoing pandemic of coronavirus disease 2019 (COVID-19). Single cell RNA sequencing (scRNAseq) studies have been valuable for studying SARS-CoV-2 pathogenesis, but the performance of these methods to detect and quantify viral RNAs has not been evaluated. Here we develop an analysis pipeline, single cell coronavirus sequencing (scCoVseq), to quantify unambiguous reads derived from coronavirus genomic (gRNA) and subgenomic mRNAs (sgmRNAs). We use this method to compare the ability of scRNAseq methods developed by 10X Genomics to detect and quantify SARS-CoV-2 RNAs, with particular focus on sgmRNAs. We find that while sequencing libraries from 10X Genomics Chromium Next Gem Single Cell V(D)J (10X 5') contain more unambiguous reads derived from sgmRNAs due to the presence of reads spanning junctions between the viral 5' leader and sgmRNA open reading frames. We demonstrate that by extending read 1 (R1) of 10X 5' leaders we can further increase the number of unambiguous reads from SARS-CoV-2 sgmRNA resulting in more UMIs per sgmRNA per cell. Using this method, which we call 10X 5' Extended R1, we are able quantify viral sgmRNA production per cell, which we believe will improve understanding regarding the dynamics of coronavirus RNA biogenesis over time and across cell types and viruses. We believe this will improve our understanding of coronavirus pathogenesis.
2023-07-30 | GSE189900 | GEO