Ontology highlight
ABSTRACT:
PROVIDER: PRJNA895061 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22069876.fastq.gz | Fastqsanger.gz | |||
| SRR22069877.fastq.gz | Fastqsanger.gz | |||
| SRR22069878.fastq.gz | Fastqsanger.gz | |||
| SRR22069879.fastq.gz | Fastqsanger.gz | |||
| SRR22069880_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Background: The recent emergence of a novel coronavirus in the Middle East (designated MERS-CoV) is a reminder of the zoonotic potential of coronaviruses and the severe disease these etiologic agents can cause in humans. Clinical features of Middle East respiratory syndrome (MERS) include severe acute pneumonia and renal failure that is highly reminiscent of severe acute respiratory syndrome (SARS) caused by SARS-CoV. The host response is a key component of highly pathogenic respiratory virus infection. Here, we computationally analyzed gene expression changes in a human airway epithelial cell line infected with two genetically distinct MERS-CoV strains obtained from human patients, MERS-CoV-EMC (designated EMC) and MERS-CoV-London (designated LoCoV). Results: Using topological techniques, such as persistence homology and filtered clustering, we characterized the host response system to the different MERS-CoVs, with LoCoV inducing early kinetic changes, between 3 and 12 hours post infection, compared to EMC. Robust transcriptional changes distinguished the two MERS-CoV strains predominantly at the late time points. Combining statistical analysis of infection and cytokine-stimulated treatment transcriptomics, we identified differential innate and pro-inflammatory responses between the two virus strains, including up-regulation of extracellular remodeling genes following LoCoV infection and differential pro-inflammatory responses between the two strains. Conclusions: These transcriptional differences may be the result of amino acid differences in viral proteins known to modulate innate immunity against MERS infection. Triplicate wells of Calu-3 2B4 cells were infected with Human Coronavirus EMC 2012 (HCoV-EMC) or time-matched mock infected. Cells were harvested at 0, 3, 7, 12, 18 and 24 hours post-infection (hpi), RNA extracted and transcriptomics analyzed by microarray.
2014-08-31 | E-GEOD-56677 | biostudies-arrayexpress
Project description:MERS-CoV and H5N1 infection
2018-01-16 | GSE108881 | GEO
Project description:Background: The recent emergence of a novel coronavirus in the Middle East (designated MERS-CoV) is a reminder of the zoonotic potential of coronaviruses and the severe disease these etiologic agents can cause in humans. Clinical features of Middle East respiratory syndrome (MERS) include severe acute pneumonia and renal failure that is highly reminiscent of severe acute respiratory syndrome (SARS) caused by SARS-CoV. The host response is a key component of highly pathogenic respiratory virus infection. Here, we computationally analyzed gene expression changes in a human airway epithelial cell line infected with two genetically distinct MERS-CoV strains obtained from human patients, MERS-CoV-EMC (designated EMC) and MERS-CoV-London (designated LoCoV). Results: Using topological techniques, such as persistence homology and filtered clustering, we characterized the host response system to the different MERS-CoVs, with LoCoV inducing early kinetic changes, between 3 and 12 hours post infection, compared to EMC. Robust transcriptional changes distinguished the two MERS-CoV strains predominantly at the late time points. Combining statistical analysis of infection and cytokine-stimulated treatment transcriptomics, we identified differential innate and pro-inflammatory responses between the two virus strains, including up-regulation of extracellular remodeling genes following LoCoV infection and differential pro-inflammatory responses between the two strains. Conclusions: These transcriptional differences may be the result of amino acid differences in viral proteins known to modulate innate immunity against MERS infection.
2014-08-31 | GSE56677 | GEO
Project description:MERS-CoV and H5N1 infection
2018-01-16 | GSE108882 | GEO
Project description:Human circular RNAs can function in competing endogenous RNA (ceRNA) network by sponging miRNA and regulating gene expression. Viruses are evolved to regulate noncoding RNAs such as miRNAs and circRNAs to facilitate their propagation and pathogenesis. Studies on how host ceRNAs upon human coronavirus infection were scarce, and the functions of circRNAs during the infection of Middle East respiratory syndrome coronavirus (MERS-CoV) has not been deeply revealed. Therefore, we conducted a whole transcriptional profile (RNA-seq) analysis to compare the expression of circRNAs, miRNAs and mRNAs between the mock-infected and MERS-CoV-infected human lung adenocarcinoma (Calu-3) cells. Integrated analysis of ceRNAs revealed putative viral pathogenic circRNAs induced by MERS-CoV and their interplay with miRNAs and genes. Our study offered new insights into the mechanisms of interplays of MERS-CoVs and hosts, and established a model promising to be applied to other coronavirus or other viruses for the identification of novel host factors.
2019-11-30 | GSE139516 | GEO
Project description:The purpose is to obtain samples for microRNA analysis in primary human airway epithelial cells infected with wild type MERS-coronavirus (MERS-CoV) (icMERS).
2016-06-09 | GSE81852 | GEO
Project description:We demonstrate that the histone demethylase KDM6A promotes infection of diverse coronaviruses, including SARS-CoV-1, SARS-CoV-2, MERS-CoV and mouse hepatitis virus (MHV) in a demethylase activity-independent manner
2023-04-10 | GSE228268 | GEO
Project description:We will use the EMC/2012 strain of the novel beta Coronavirus called Middle East Respiratory Syndrome Coronavirus (MERS-CoV). It was initially passaged on Vero E6 cells in Saudi Arabia before being sequenced at the Erasmus Medical College in Rotterdam, Netherlands by Dr Ron Fouchier. We propose to perform a time course of infection of hCoV-EMC on MRC5 cells (Human Lung origin) and Vero cells (African Green Monkey Kidney cells). Both cell lines readily grow and replicate the virus. Importantly these cell lines show signs of Cytopathic effect (CPE), such as cell rounding and release from the petri dish that coincide with time points high virus replication demonstrating the effects of virus replication on the cells. Transcriptomic analysis will be performed after infection with MERS-CoV and SARS-CoV (Urbani strain) to compare the host gene induction that occurs during infection. MRC5 and Vero E6 cells will be infected at an MOI of 0.1 and 3 and RNA harvested from cells at 24 and 48 post infection. RNA will be processed for library creation and sequenced on an Illumina Hiseq. Sequencing reads will be analyzed and compared across the time course and between each virus to identify common response pathways induced during infection as well as unique pathways specific to each virus.
2015-11-19 | E-GEOD-56193 | biostudies-arrayexpress
Project description:MERS-CoV genome-derived small RNAs in Huh7 cells infected with a Korean isolate of MERS-CoV (KNIH002; Genbank accession no. KT029139.1)
2023-04-17 | GSE148860 | GEO
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