Ontology highlight
ABSTRACT:
PROVIDER: PRJNA683133 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In this study, we used RNA-sequencing to compare the transcriptional programmes in cESC, elicited either by stimulation with recombinant interferon-α or by infection with the attenuated Fowlpox virus vaccine strain (FP9), the canarypox virus vaccine strain (CNPV), the Modified Vaccinia Ankara (MVA) virus or PBG98, a mild vaccine strain of infectious bursal disease virus.
2019-05-09 | GSE127203 | GEO
Project description:Fowlpox virus (here as FP9, a plaque-purified, high passage-attenuated derivative) effectively suppresses induction of the âinnateâ immune responses, notably the Type I interferon system, of the permissive host (chicken). Despite the extensive usage of fowlpox virus as a recombinant vaccine vector in chickens, its immunomodulatory mechanisms remain largely unknown. In this study, a transcriptomic analysis using the Affymetrix GeneChip chicken genome array was performed at the host gene transcription level at 4, 8, 16 and 24 hours post-infection of mock treated and FP9-infected (MOI=5, 2h) chicken embryo fibroblasts (CEF). The experiment was performed in triplicate with three different batches of CEFs. Because fowlpox virus is capable of expressing antigens in mammalian cells, these studies in chicken cells form a baseline for subsequent study of immunomodulation of mammalian innate immune responses.
2018-12-31 | E-MTAB-5455 | biostudies-arrayexpress
Project description:Fowlpox virus strain:282E4 Genome sequencing
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Project description:Complete genome sequencing of fowlpox virus
| PRJNA1295713 | ENA
Project description:Fowlpox virus strain:Vaccine | isolate:FPV_MGH-AD02 Genome sequencing and assembly
| PRJNA1401287 | ENA
Project description:Fowlpox virus (FWPV) is a double-stranded DNA virus, used as a live vaccine against poultry diseases, and considered a promising potential mammalian vaccine vector. Similar to mammalian poxviruses, FWPV has evolved mechanisms to evade host immune responses at different levels. We infected chicken embryo fibroblasts (CEF) with individual FWPV mutants (n=59), each deficient in one non-essential gene, from a previously described knock-out virus library [Laidlaw et al, 2013 J Virology 87(9); Laidlaw and Skinner, 2014 Bio-protocol 4(10); e1126]. Host responses to the mutant viruses were screened at 16h post infection for each virus using Affymetrix GeneChip Genome arrays which includes probes for most FWPV genes. Controls included the wild type virus and uninfected samples. To avoid systematic errors due to different batches of CEF and hybridisation/scanning on different dates, samples were processed in groups of randomised samples.
2019-01-01 | E-MTAB-7276 | biostudies-arrayexpress
Project description:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Primary endpoints: circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
| 2533916 | ecrin-mdr-crc
Project description:Long-range RNA-RNA pairing impacts the genome structure and function of SARS-CoV-2 variants. To understand structure and function relationships of different SARS-CoV-2 variants that have emerged during the COVID-19 pandemic, we performed high throughput structure probing and modelling of the genomic structures of the wildtype (WT), Alpha, Beta, Delta and Omicron variants of the SARS-CoV-2. We observed that genomes of SARS-CoV-2 variants are generally structurally conserved, and that single nucleotide variations (SNVs) and interactions with RNA binding proteins (RBPs) can impact RNA structures across the viruses. Importantly, using proximity ligation sequencing, we identified many conserved ultra-long-range RNA-RNA interactions, including one that spans more than 17kb in both the WT virus and Omicron variant. We showed that mutations that disrupt this 17kb long-range interacting structure reduce virus fitness at late stages of its infection cycle, while compensatory mutations partially restore virus fitness. Additionally, we showed that this ultra-long-range RNA-RNA interaction binds directly to ADAR1 to alter the RNA editing levels on the viral genome. These studies deepen our understanding of RNA structures in SARS-CoV-2 genome and their ability to interact with host factors to facilitate virus infectivity.
2025-07-30 | PXD065815 | JPOST Repository
Project description:Human cells identify invading pathogens and activate immune signaling pathways through a wide array of pattern recognition receptors, such as DNA sensors. The interferon-inducible protein 16 (IFI16) is a nuclear DNA sensor that recognizes double-stranded DNA from a number of viral sources, including genomes of nuclear-replicating viruses such as the prevalent human pathogen, herpes simplex virus 1 (HSV-1). Upon binding to the DNA genome of HSV-1, IFI16 both induces antiviral cytokine expression and suppresses virus gene expression. Here, we use a multi-omics approach of DNA sequencing techniques paired with targeted mass spectrometry to obtain an extensive view of the interaction between IFI16 and the HSV-1 genome, and how this binding affects the viral DNA structure and protein expression. Through ChIP-seq, we find that IFI16 binds to the HSV-1 genome in a sequence-independent manner while simultaneously exhibiting broad enrichment at two loci: UL30, the viral DNA polymerase gene, and US1-US7. ATAC-seq analysis reveals that these two regions are among the most accessible stretches of DNA on the genome, thereby facilitating IFI16 binding. Accessibility of the entire HSV-1 genome is elevated upon IFI16-KO, indicating that expression of IFI16 globally induces chromatinization of viral DNA, regardless of IFI16 enrichment. Deletion of IFI16 also results in a global increase in the expression of HSV-1 proteins, as measured by parallel reaction monitoring-mass spectrometry. Altogether, we demonstrate that IFI16 interacts with the HSV-1 genome in a sequence-independent manner, and this interaction coordinates epigenetic silencing of the viral genome, resulting in decreased protein expression and virus replication.
2022-04-27 | PXD031850 | panorama