Avian paramyxovirus 1 strain:Komarov
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ABSTRACT:
PROVIDER: PRJNA1123209 | ENA |
REPOSITORIES: ENA
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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.
2012-08-15 | GSE40100 | GEO
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 (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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Project description:Newcastle Disease Virus samples from outbreaks in 1951-2015 in West Java, Indonesia
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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).
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Project description:Newcastle disease virus (NDV) is an avian paramyxovirus that causes major economic losses to the poultry industry around the world, with NDV pathogenicity varying due to strain virulence differences. However, the impact of intracellular viral replication and the heterogeneity of host responses among cell types are unknown. Here, we investigated the heterogeneity of lung tissue cells in response to NDV infection in vivo and that of chicken embryo fibroblast cell line DF-1 to NDV infection in vitro using single-cell RNA sequencing.
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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