Ontology highlight
ABSTRACT:
PROVIDER: PRJNA953504 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24109053.fastq.gz | Fastqsanger.gz | |||
| SRR24109054.fastq.gz | Fastqsanger.gz | |||
| SRR24109055.fastq.gz | Fastqsanger.gz | |||
| SRR24109056.fastq.gz | Fastqsanger.gz | |||
| SRR24109057.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the role of gene expression during Newcastle disease virus (NDV) infection.The NDV GM strain was used to infect DEF cells with 1moi, while an uninfected group was set up as a control.
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Project description:The NDV GM strain was used to infect DEF cells with 1moi, while an uninfected group was set up as a control. Changes in transcript levels of different genes after NDV infection of duck cells were identified by high-throughput sequencing. It is hoped to reveal the unique antiviral mechanism of waterfowl in resisting NDV infection.
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Project description:To investigate the role of m6A modification during Newcastle disease virus (NDV) infection We then performed gene expression profiling analysis using data obtained from RNA-seq and MeRIP-seq of NDV infected CEF cells and normal cells.
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Project description:Newcastle disease virus (NDV) has emerged as an oncolytic agent in several cancers. Previous study has shown that NDV exerts cytolytic activity in glioma, however, the underlying mechanism has not been fully uncovered. Here the cytolytic activity of NDV in glioma and the associated mechanisms have been demonstrated. Infection with NDV inhibits cell proliferation and promotes cell apoptosis in LN229 cells. Further investigation showed that cytoplasmic organelle damage and cytoplasmic vacuolation were observed in LN229 cells after NDV infection. JC-1 staining assay proved that NDV caused cell apoptosis of LN229 cells by inducing mitochondrial dysfunction. We next speculated that NDV caused LN229 cells death through inducing necroptosis, but not ferroptosis, since the Fe2+ level did not alter after NDV infection. Furthermore, the NDV-caused cell death in LN229 cells was blocked by necroptosis inhibitor Nec1. Besides, RNA-seq analysis identified the different expression genes in NDV-infected LN229 cells. OASL, an antiviral gene, has been found to be directly induced by NDV infection. We also found that knockdown of OASL enhanced NDV infection-induced LN229 cells necroptosis. In summary, two aspects about cytolytic activity of NDV in glioma have been demonstrated. NDV presented cytolytic activity in glioma cells through inducing necroptosis. Additionally, targeting OASL may provide new strategy for enhancing necroptosis of glioma cells after NDV infection.
2023-05-01 | GSE227791 | GEO
Project description:Three small RNA libraries constructed from uninfected HeLa cells or the cells infected with NDV strain Herts/33 at 6 and 12 hr post inoculation were sequenced using an Illumina platform.Three replicates of each group (Mock, NDV-6h and NDV-12h) were prepared and pooled separately for library construction and small RNA Deep sequencing.
2020-11-08 | E-MTAB-9690 | biostudies-arrayexpress
Project description:Genotype VIId NDV is characterized by severe tissue damage in chicken lymphoid organs compared to other virulent strains. However, biological basis of this unusual pathological phenotype is unknown. Host response is associated with pathogenicity of Newcastle Disease Virus (NDV). We aim to determine the contribution of host response to the severe tissue destruction in the lymphoid system caused by genotype VIId NDV. We used microarray analysis to evaluate the global transcriptional response in the spleen of chickens infected with genotype VIId NDV strain JS5/05 and genotype IV NDV Herts/33.
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Project description:Nuclear localization of cytoplasmic RNA virus proteins mediated by intrinsic nuclear localization signal (NLS) plays essential roles in successful virus replication. We previously reported that NLS mutation in the matrix (M) protein obviously attenuates the replication and pathogenicity of Newcastle disease virus (NDV), but the attenuated replication mechanism of NDV remains unclear. In this study, we showed that M/NLS mutation not only disrupted M’s nucleocytoplasmic trafficking characteristic but also impaired viral RNA synthesis and transcription. Using TMT-based quantitative proteomics analysis of BSR-T7/5 cells infected with the parental NDV rSS1GFP and the mutant NDV rSS1GFP-M/NLSm harboring M/NLS mutation, we found that rSS1GFP infection stimulated much greater quantities and more expression level changes of differentially expressed proteins involved in host cell transcription, ribosomal structure, posttranslational modification, and intracellular trafficking than rSS1GFP-M/NLSm infection. Further in-depth analysis revealed that early nuclear localization of M protein inhibited cell transcription and participated in reducing cellular protein synthesis, posttranscriptional modification and transport; whereas later cytoplasmic localization of M protein promoted viral protein synthesis and benefited for virus assembly and budding. Importantly, we first demonstrated that later cytoplasmic localization of M protein effected the inhibition of TIFA expression in a dose-dependent manner, and inhibiting TIFA expression was beneficial to NDV replication by down-regulating TIFA/TRAF6/NF-κB-mediated production of cytokines. Our findings suggest that precocious cytoplasmic localization of M protein caused by M/NLS mutation disrupts these important biological processes, and thereby causes the attenuated replication of NDV, demonstrating that NDV replication is closely related to the nucleocytoplasmic trafficking of M protein.
2020-05-22 | PXD018098 | Pride
Project description:Genotype VIId NDV is characterized by severe tissue damage in chicken lymphoid organs compared to other virulent strains. However, biological basis of this unusual pathological phenotype is unknown. Host response is associated with pathogenicity of Newcastle Disease Virus (NDV). We aim to determine the contribution of host response to the severe tissue destruction in the lymphoid system caused by genotype VIId NDV. We used microarray analysis to evaluate the global transcriptional response in the spleen of chickens infected with genotype VIId NDV strain JS5/05 and genotype IV NDV Herts/33. Chickens were inoculated with JS5/05 or Herts/33 or mock-infected. At day 2 post infection, spleens were isolated from three chickens per group for RNA extraction and hybridization on Affymetrix microarrays. Samples were named as follows: JS5/05 (I4_1_NS,I4_2_NS,I4_3_NS), Herts/33 (H1_NS,H2_NS, H3_NS), control (C1_NS, C2_NS, C3_NS).
2012-08-14 | E-GEOD-40100 | biostudies-arrayexpress
Project description:Newcastle disease (ND) affects a few hundred avian species including chicken, and the clinical outcome of Newcastle disease virus (NDV) infection ranges from mild to severe fatal disease depending on the NDV pathotype and the host species involved. Japanese quails serve as natural reservoirs of NDV and play important role in NDV epidemiology. While infection of chicken with velogenic NDV results in severe often fatal illness, the same infection in Japanese quails is results in in apparent infection. The molecular basis of this contrasting clinical outcomes of NDV infection is not yet known. We compared global gene expression in spleens of chicken and Japanese quails infected with a lentogenic or velogenic NDVs. We found contrasting regulation of key genes associated with NF-κB pathway and T-cell activation between chicken and Japanese quails. Our data suggests association of NDV resistance in Japanese quails to activation of NF-κB pathway and T cell proliferation.
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