Small noncoding RNA Expression Following Respiratory Syncytial Virus or Measles Virus Infection of Neuronal Cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE167724 | GEO | 2021/09/22
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptional responses in lungs of mice infected with Respiratory Syncytial Virus (RSV) were compared to a control and mock infections
2007-04-17 | E-TABM-221 | biostudies-arrayexpress
Project description:Small noncoding RNA Expression Following Respiratory Syncytial Virus or Measles Virus Infection of Neuronal Cells
| PRJNA705182 | ENA
Project description:In this study we investigated whether there exists a genomic signature that can accurately predict the course of a respiratory syncytial virus (RSV) infection in hospitalized young infants. We used early blood microarray transcriptome profiles from 39 infants that were followed until recovery and of which the level of disease severity was determined retrospectively. Applying support vector machine learning on age by sex standardized transcriptomic data, an 84 gene signature was identified that discriminated hospitalized infants with eventually less severe RSV infection from infants that suffered from most severe RSV disease.
2016-11-11 | E-MTAB-5195 | biostudies-arrayexpress
Project description:Stimulation of unmyelinated C-fibers is able to initiate host responses. In this study, we established the model of C fiber degenerated (KPCF) mice. KPCF mice were given respiratory syncytial virus (RSV) infection. We aimed to figure out the role of C fibers in RSV infection.
2022-10-11 | GSE215099 | GEO
Project description:A measles virus (MeV) isolate bearing a single amino acid change in the fusion protein (F) -- L454W -- was identified in two patients who died of MeV central nervous system (CNS) infection. We analyzed whether this mutation confers an advantage over wild type virus in the CNS, thereby contributing to disease in these patients. Using murine ex vivo organotypic brain cultures and human induced pluripotent stem cell-derived brain organoids, we show that specific CNS adaptive mutations in F result in augmented spread of virus ex vivo and that this is associated with an enhanced innate immune response. The spread of virus in brain organoids is blocked by an inhibitory peptide that targets F, confirming that dissemination in the brain tissue is attributable to F. A single mutation in MeV F thus alters the fusion complex to render the virus more neuropathogenic, allowing it to propagate in the face of the innate immune response.
2020-08-08 | GSE155885 | GEO
Project description:A measles virus (MeV) isolate bearing a single amino acid change in the fusion protein (F) -- L454W -- was identified in two patients who died of MeV central nervous system (CNS) infection. We analyzed whether this mutation confers an advantage over wild type virus in the CNS, thereby contributing to disease in these patients. Using murine ex vivo organotypic brain cultures and human induced pluripotent stem cell-derived brain organoids, we show that specific CNS adaptive mutations in F result in augmented spread of virus ex vivo and that this is associated with an enhanced innate immune response. The spread of virus in brain organoids is blocked by an inhibitory peptide that targets F, confirming that dissemination in the brain tissue is attributable to F. A single mutation in MeV F thus alters the fusion complex to render the virus more neuropathogenic, allowing it to propagate in the face of the innate immune response.
2020-08-08 | GSE155884 | GEO
Project description:The major inducible 70 kDa heat shock protein (hsp70) is host protective in a mouse model of measles virus (MeV) brain infection. Transgenic constitutive expression of hsp70 in neurons, the primary target of MeV infection, abrogates neurovirulence in neonatal H-2d congenic C57BL/6 mice. A significant level of protection is retained after depletion of T lymphocytes, implicating innate immune mechanisms. Focus of the present work was to elucidate the basis for hsp70-dependent innate immunity using this model. Transcriptome analysis of brains from transgenic (TG) and non-transgenic (NT) mice 5 days after infection identified type 1 interferon (IFN) signaling and macrophage activation/antigen presentation as the main differences linked to survival. The pivotal role for type 1 IFN in hsp70-mediated protection was demonstrated in mice with a genetically disrupted type 1 IFN receptor (IFNAR-/-), where IFNAR-/- eliminated the difference in survival between TG and NT mice. Brain macrophages, not neurons, are the predominant source of type 1 IFN in the virus-infected brain, and in vitro studies provided a mechanistic basis by which MeV-infected neurons can induce IFN-β in uninfected microglia in an hsp70-dependent manner. MeV infection induced extracellular release of hsp70 from mouse neuronal cells that constitutively express hsp70, and extracellular hsp70 induced IFN-β transcription in mouse microglial cells through Toll-like receptors 2 and 4. Collectively, results support a novel axis of type 1 IFN-dependent antiviral immunity in the virus-infected brain that is driven by hsp70.
2012-11-14 | GSE42264 | GEO
Project description:Measles virus infects serum activated airway epithelial cells and many adenocarcinoma cell lines. A microarray analysis was performed on virus permissive versus non-permissive cells. Membrane protein genes that were upregulated in permissive cells were tested as receptor/entry factors. Membrane protein genes that were upregulated in smooth airway epithelial cells (SAEC) following growth in 10% fetal calf serum that made the cell line permissive to measles virus were identified. Membrane protein genes that were upregulated in adenocarcinoma cells that were permissive to wild type measles virus infection were identified.
2011-07-29 | GSE26636 | GEO
Project description:The major inducible 70 kDa heat shock protein (hsp70) is host protective in a mouse model of measles virus (MeV) brain infection. Transgenic constitutive expression of hsp70 in neurons, the primary target of MeV infection, abrogates neurovirulence in neonatal H-2d congenic C57BL/6 mice. A significant level of protection is retained after depletion of T lymphocytes, implicating innate immune mechanisms. Focus of the present work was to elucidate the basis for hsp70-dependent innate immunity using this model. Transcriptome analysis of brains from transgenic (TG) and non-transgenic (NT) mice 5 days after infection identified type 1 interferon (IFN) signaling and macrophage activation/antigen presentation as the main differences linked to survival. The pivotal role for type 1 IFN in hsp70-mediated protection was demonstrated in mice with a genetically disrupted type 1 IFN receptor (IFNAR-/-), where IFNAR-/- eliminated the difference in survival between TG and NT mice. Brain macrophages, not neurons, are the predominant source of type 1 IFN in the virus-infected brain, and in vitro studies provided a mechanistic basis by which MeV-infected neurons can induce IFN-β in uninfected microglia in an hsp70-dependent manner. MeV infection induced extracellular release of hsp70 from mouse neuronal cells that constitutively express hsp70, and extracellular hsp70 induced IFN-β transcription in mouse microglial cells through Toll-like receptors 2 and 4. Collectively, results support a novel axis of type 1 IFN-dependent antiviral immunity in the virus-infected brain that is driven by hsp70. Hsp70 expression in mice enhances gene expression related to antiviral immune response against MeV neurovirulence. We performed microarrays on whole brain tissues in mice to obtain an unbiased picture of how hsp70 alters host innate responses to viral infection. Hsp70-overexpressing transgenic (TG) and non-transgenic (NT) mice were infected with MeV intracranially, and total brain mRNA harvested at 5 and 10 days post infection (d.p.i.) was analyzed, sampling the hemisphere opposite the side of viral inoculation. Analysis includes 6 groups: infected TG at 5 d.p.i. (n=4), infected TG at 10 d.p.i. (n=5), infected NT at 5 d.p.i. (n=4), infected NT at 10 d.p.i. (n=5), uninfected TG at 5 d.p.i. (n=4), and uninfected NT at 5 d.p.i. (n=4).
2012-11-14 | E-GEOD-42264 | biostudies-arrayexpress
Project description:Respiratory syncytial virus (RSV) is a major cause of morbidity and mortality. Previous studies have suggested that T cell responses may contribute to RSV immunopathology, which could be driven by dendritic cells (DCs). DCs are productively infected by RSV, and during RSV infections, there is an increase of DCs in the lungs with a decrease in the blood. Pediatric populations are particularly susceptible to severe RSV infections, however DC responses to RSV from pediatric populations have not been examined. In this study, primary isolated DCs from cord blood and adult peripheral blood were compared after RSV-infection. Transcriptional profiling and biological network analysis identified transforming growth factor (TGF)-b and associated signaling molecules as differentially regulated in the two age groups. TGF-b1 was decreased in RSV-infected adult blood DCs, but increased in RSV-infected cord blood DCs. Co-culture of adult RSV-infected DCs with autologous T-cells induced secretion of interferon gamma (IFNg), IL-12p70, IL-2, and tumor necrosis factor alpha (TNFa). Conversely, co-culture of cord RSV-infected DCs and autologous T-cells induced secretion of IL-4, IL-6, IL-1b, and IL-17. Addition of purified TGF-b1 to adult DC-T cell co-cultures reduced secretion of IFNg, IL-12p70, IL-2, and TNFa, which addition of a TGF-b chemical inhibitor to cord DC-T cell co-cultures increased secretion of IL-12p70. These data suggest that TGF-b acts as a major regulator of RSV DC-T cell responses, which could contribute to immunopathology during infancy. Three sets of adult peripheral DCs were analyzed and three sets of cord blood DCs. The DCs from each donor were divided in half and either mock infected or infected with RSV and each (12 samples total) were used for affymetrix array analsis. The donor-matched mock infected DC hybridyzation was used as the reference sample for the RSV infected.
2010-11-01 | E-GEOD-24132 | biostudies-arrayexpress