Ontology highlight
ABSTRACT:
PROVIDER: PRJEB42421 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR5195170_1.fastq.gz | Fastqsanger.gz | |||
| ERR5195170_2.fastq.gz | Fastqsanger.gz | |||
| ERR5195180_1.fastq.gz | Fastqsanger.gz | |||
| ERR5195180_2.fastq.gz | Fastqsanger.gz | |||
| ERR5195190_1.fastq.gz | Fastqsanger.gz |
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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: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:Acute kidney injury is strongly associated with mortality in COVID-19 patients. However, host cell changes underlying infection of kidney cells with SARS-CoV-2 remain unknown and prevent understanding of the mechanisms leading to renal pathology. Here, we carried out extensive, dual-level proteomic analyses of primary human kidney cells infected with SARS-CoV-2 or MERS-CoV to disseminate virus and cell type specific changes. We established cellular infection models of proximal and distal tubular epithelial cells derived from human donors. Infected cells were analyzed by quantitative translatome and whole-cell proteomics over time. Our findings reveal shared pathways modified upon infection with both viruses, as well as SARS-CoV-2 specific host cell modulation driving key changes in innate immune activation, cellular protein quality control and mitochondrial biology. In addition, we identified extensive modulation in pathways associated with kidney failure that were instinctively regulated in a virus- and cell type-specific manner. Our findings provide an overview of the effects of SARS-CoV-2 or MERS-CoV infection on primary kidney cells revealing key pathways and highlighting potential treatment options.
2022-01-30 | PXD024398 | Pride
Project description:Middle East respiratory syndrome coronavirus (MERS-CoV) is a beta coronavirus that emerged in 2012, causing severe pneumonia and renal failure. MERS-CoV encodes five accessory proteins. Some of them have been shown to interfere with host antiviral immune response. However, the roles of protein 8b in innate immunity and viral virulence was rarely studied. Here, we introduced individual MERS-CoV accessory protein genes into the genome of an attenuated murine coronavirus (Mouse hepatitis virus, MHV), respectively and found accessory protein 8b could enhance viral replication in vivo and in vitro, and increase the lethality of infected mice. RNA-seq analysis revealed that protein 8b could significantly inhibit type I interferon production (IFN-I) and innate immune response in mice infected with MHV expressing protein 8b. We also found that MERS-CoV protein 8b could initiate from multiple internal methionine sites and at least three protein variants were identified. Residues 1-23 of protein 8b was demonstrated to be responsible for increased virulence in vivo. In addition, the inhibitory effect on IFN-I of protein 8b might not contribute to its virulence enhancement as aa1-23 deletion did not affect IFN-I production in vitro and in vivo. Next, we also found that protein 8b was localized to the endoplasmic reticulum (ER)/Golgi membrane in infected cells, which was disrupted by C-terminal region aa 88-112 deletion. This study will provide new insight into the pathogenesis of MERS-CoV infection.
2021-11-16 | GSE188514 | GEO
Project description:Host kinases play essential roles in the host cell cycle, innate immune signaling, the stress response to viral infection, and inflammation. Previous work has demonstrated coronaviruses specifically target kinase cascades to subvert host cell responses to infection and rely upon host kinase activity to phosphorylate viral proteins to enhance replication. Given the number of kinase inhibitors that are already FDA approved to treat cancers, fibrosis, and other human disease, they represent an attractive class of compounds to repurpose for host targeted therapies against emerging coronavirus infections. To further understand the host kinome response to betacoronavirus infection we employed multiplex inhibitory bead mass spectrometry (MIB-MS) following MERS-CoV and SARS-CoV-2 infection of human lung epithelial cell lines. Our MIB-MS analyses revealed activation of mTOR and MAPK signaling following MERS-CoV and SARS-CoV-2 infection, respectively.
2023-08-01 | PXD040901 | Pride
Project description:Bat cells and tissue have elevated basal expression levels of antiviral genes commonly associated with IFNα signalling. Here we show IRF1,3 and 7 levels are elevated in most bat tissues and that basally, IRFs contribute to the expression of type I IFN ligands and high expression of Interferon Regulated Genes (IRGs). CRISPR KO of IRF 1/3/7 in cells reveal distinct subsets of genes affected by each IRF in an IFN-ligand signalling dependent and largely independent manner. As the master regulators of innate immunity, the IRFs, control the kinetics and maintenance of the IRG response and play essential roles in response to IAV, HSV1, PRV3M and MERS-CoV infection. With its differential expression compared to human, this highlights a critical role for basal IRF expression in viral responses and potentially immune cell development in bats with relevance for IRF function in human biology.
2020-10-23 | PXD021982 | JPOST Repository
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes Coronavirus disease 2019 (COVID-19) has caused a global health emergency. A key feature of COVID-19 is dysregulated Interferon-response. Type-I interferon (IFN-I) is one of the earliest antiviral innate immune responses following viral infection and plays a significant role in pathogenesis of SARS-CoV-2. In this study, using a proteomics-based approach, we identified that SARS-CoV-2 infection induces delayed and dysregulated IFN-I signaling in Huh7 cells. We demonstrate that SARS-CoV-2 is able to inhibit RIG-I mediated IFN- production. Our results also confirm the recent findings that IFN-I pretreatment is able to reduce susceptibility of Huh7 cells to SARS-CoV-2, but not post-treatment. Senescent Huh7 cells in spite of showing accentuated IFN-I response were more susceptible to SARS-CoV-2 infection and SARS-CoV-2 effectively inhibited IFIT1 in these cells. Proteomic comparison between SARS-CoV-2, SARS-CoV and MERS-CoV revealed a distinct differential regulatory signature of interferon-related proteins emphasizing that therapeutic strategies based on observations in SARS-CoV and MERS-CoV should be used with caution. Our findings provide a better understanding of SARS-CoV-2 regulation of cellular interferon response and a perspective on its use as a treatment. Characterization of the role of different interferon stimulated genes on the inhibition of SARS-CoV-2 pathogenesis may direct novel antiviral strategies.
2021-05-18 | PXD023450 | Pride
Project description:Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Recently we could show that the SARS-CoV-2 spike protein (S-protein) primes inflammasome formation and release of mature interleukin-1β (IL-1β) in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naïve individuals (Theobald et al. EMBO Mol Med. 2021). Further analysis revealed that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling. In this project we want to focus on novel mRNA vaccines, which are exploiting S-protein driven immunogenicity for protection against SARS-CoV-2. Transcriptome analyses of macrophages might reveal differences in innate immune-associated pathways between vaccinated and unvaccinated individuals after prime-boost. Thus, our project could help to gain a better understanding of vaccine-induced immunity including underlying molecular mechanisms in the interaction of the innate and adaptive immune system after mRNA-based SARS-CoV-2 vaccination.
2022-05-02 | GSE200274 | GEO
Project description:MERS-CoV and H5N1 infection
2018-01-16 | GSE108881 | GEO
Project description:All respiratory viruses establish primary infections in the nasal epithelium, where efficient innate immune induction may prevent dissemination to the lower airway and thus minimize pathogenesis. Human coronaviruses (HCoVs) cause a range of pathologies, but the host and viral determinants of disease during common cold versus lethal HCoV infections are poorly understood. We model the initial site of infection using primary nasal epithelial cells cultured at air-liquid interface (ALI). HCoV-229E, HCoV-NL63 and human rhinovirus-16 are common cold-associated viruses that exhibit unique features in this model: early induction of antiviral interferon (IFN) signaling, IFN-mediated viral clearance, and preferential replication at nasal airway temperature (33ºC) which confers muted host IFN responses. In contrast, lethal SARS-CoV-2 and MERS-CoV encode antagonist proteins that prevent IFN-mediated clearance in nasal cultures. Our study identifies features shared among common cold-associated viruses, highlighting nasal innate immune responses as predictive of infection outcomes and nasally-directed IFNs as potential therapeutics.
2024-03-25 | GSE253542 | GEO