Severe acute respiratory syndrome coronavirus 2
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ABSTRACT:
PROVIDER: PRJNA667798 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:2019 novel coronavirus
| PRJNA605907 | ENA
Project description:The ongoing pandemic of coronavirus disease 2019 (COVID-19), which results from the rapid spread of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a significant global public health threat, with molecular mechanisms underlying its pathogenesis largely unknown. Small non-coding RNAs (sncRNAs) are known to play important roles in almost all biological processes. In the context of viral infections, sncRNAs have been shown to regulate the host responses, viral replication, and host-virus interaction. Compared with other subfamilies of sncRNAs, including microRNAs (miRNAs) and Piwi-interacting RNAs (piRNAs), tRNA-derived RNA fragments (tRFs) are relatively new and emerge as a significant regulator of host-virus interactions. Using T4 PNK‐RNA‐seq, a modified next‐generation sequencing (NGS), we recently found that nasopharyngeal swabs (NPS) samples from SARS-CoV-2 positive and negative subjects show a significant difference in sncRNA profiles. There are about 166 SARS-CoV- 2-impacted sncRNAs. Among them, tRFs are the most significantly affected and almost all impacted tRFs are derived from the 5’-end of tRNAs (tRF5). Using a modified qRT-PCR, which was recently developed to specifically quantify tRF5s by isolating the tRF signals from its corresponding parent tRNA signals, we validated that tRF5s derived from tRNA GluCTC (tRF5-GluCTC), LysCTT (tRF5-LysCTT), ValCAC (tRF5-ValCAC), CysGCA (tRF5-CysGCA) and GlnCTG (tRF5-GlnCTG) are enhanced in NPS samples of SARS-CoV2 patients and SARS-CoV2-infected airway epithelial cells. In addition to host-derived ncRNAs, we also identified several sncRNAs derived from the virus (svRNAs), among which a svRNA derived from CoV2 genomic site 346 to 382 (sv-CoV2-346) has the highest expression. The induction of both tRFs and sv-CoV2-346 has not been reported previously, as the lack of the 3’-OH ends of these sncRNAs prevents them to be detected by routine NGS. In summary, our studies demonstrated the involvement of tRFs in COVID-19 and revealed new CoV2 svRNAs.
2022-03-01 | GSE193555 | GEO
Project description:Whole Genome Sequencing of SARS-CoV-2 from Pahang, Malaysia
| PRJNA739246 | ENA
Project description:Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo [1,2]. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE, with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigarcin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a meassure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE. We used Affymetrix microarrays (Human Genome U133 plus 2.0) to compare global gene expression between SARS-CoV-infected, mock-infected and SARS-CoV-ΔE-infected cells. For ech type of sample three hybridizations were carried-out (independent biological replicates).
2012-06-20 | E-GEOD-30589 | biostudies-arrayexpress
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genome sequencing
| PRJNA613958 | ENA
Project description:The absence of a robust disease model currently hinders the evaluation of countermeasures for Middle East respiratory syndrome coronavirus (MERS-CoV). While a rhesus macaque model of MERS-CoV that results in mild-to-moderate disease has been utilized to describe the pathogenesis of this virus and for the evaluation of therapeutics, the inability to produce uniform disease with substantial virus replication complicates analysis in countermeasure studies. In an attempt to identify a more robust disease model, DPP4 sequences of various non-human primates were aligned. Modeling of the interactions between the receptor binding domain of MERS-CoV and its cognate receptor DPP4 predicted a "good fit" with complete conservation of all of the critical residues. To determine the feasibility of the marmoset as a MERS-CoV disease model, common marmosets were inoculated with MERS-CoV via combined intratracheal, intranasal, oral and ocular routes. Marmosets developed signs of moderate to severe illness with progressive serious to severe pneumonia. Progressive gross lesions were evident in animals necropsied at 3, 4 and 6 days post inoculation and two animals were euthanized during the study due to disease severity. This is the first description of a moderate-to-severe, with potentially lethality, disease model of MERS-CoV and as such will have utility for vaccine and other countermeasure efficacy evaluations in addition to further pathogenesis studies. Lung tissue samples were isolated and sequenced at 3, 4 and 6 days post inoculation. Two animals were euthanized during the study due to disease severity.
2014-06-10 | E-GEOD-55023 | biostudies-arrayexpress
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: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.
2014-06-10 | GSE56192 | 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:Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo [1,2]. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE, with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigarcin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a meassure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE.
2012-06-21 | GSE30589 | GEO