Human respiratory syncytial virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1224818 | ENA |
REPOSITORIES: ENA
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Project description:Human Respiratory Syncytial Virus (hRSV) is a prevalent pathogen posing significant risks to infants and older adults. While the roles of RSV non-structural proteins NS1 protein in modulating host immune responses remains poorly defined, its potential impact on viral pathogenicity is critical. We employed CUT&RUN of NS1, Mediator, and ATF3 in WT NS1 and mutant NS1 expressing A549 cells and bulk RNA sequencing of WT and mutant NS1-expressing A549 (GSE155151) and RSV infection in human lung air-liquid interface (ALI) cultures to elucidate the perterbations of transcriptional regulatory control induced by NS1. Coupled with our earlier work, these epigenomic and transcriptomic profiling datasets provides deeper insights into the molecular mechanisms through which RSV NS1 protein disrupts host immune functions.
2025-03-09 | GSE270463 | GEO
Project description:Respiratory syncytial virus (RSV) causes severe disease mostly in infants; however, mechanisms of age association remain elusive. Here, employing human bronchial epithelium models generated from tracheal aspirate-derived basal stem cells of neonates and adults, we investigate whether age regulates RSV-epithelium interaction to determine disease severity. We show that following RSV infection, only neonatal epithelium model exhibits cytopathy and mucus hyperplasia, and neonatal epithelium has more robust viral spread and inflammatory responses than adult epithelium. Mechanistically, RSV-infected neonatal ciliated cells display age-related impairment of STAT3 activation, rendering susceptibility to apoptosis, which facilitates viral spread. In contrast, SARS-CoV-2 infection of ciliated cells has no effect on STAT3 activation and is not affected by age. Taken together, our findings identify an age-related and RSV-specific interaction with neonatal bronchial epithelium that critically contributes to severity of infection, and STAT3 activation offers a potential strategy to battle severe RSV disease in infants.
2024-09-01 | GSE242397 | GEO
Project description:Purpose: To understand how dexamethasone has beneficial effects on reducing mucus production but inhibits viral defense mechanisms Methods: RSV-infected mouse lungs and various cell lines, plus and minus dexamethason, were examined by RNAseq, and pathway analysis of differentially-expressed genes were compared Results: Using RNA-seq we identified a subset of cytokines that were induced by RSV and repressed by dexamethasone. Interestingly, while RSV induced interferons (IFNs) and IFN stimulated genes (ISGs), dexamethasone treatment did not affect the expression of these genes or antiviral IFN signaling pathways as has been observed with glucocorticoid treatment of other respiratory viruses [13]. Using an unbiased approach, we found that certain RSV-driven gene expression networks and genes were specifically modulated by dexamethasone treatment. Importantly, dexamethasone also reduced RSV clearance in vivo, which correlated with a reduction in specific immune response markers. Conclusion: Our results support the possibility that the beneficial anti-inflammatory effects of dexamethasone treatment are counterbalanced by the increased viral load in patients, accounting for the lack of clinical benefit derived from treatment during RSV infection.
2019-11-19 | GSE140226 | GEO
Project description:Respiratory syncytial virus (RSV) is a seasonal respiratory pathogen that primarily affects young children, potentially causing severe lower respiratory tract disease. Despite the high disease burden, understanding of RSV pathophysiology remains limited. To address this, advanced RSV infection models are needed. While HEp-2 cells are widely used due to their high susceptibility to RSV, they do not accurately reflect the host response of the human respiratory tract. In this study, we evaluated human induced pluripotent stem cell-derived respiratory organoids, which contain respiratory epithelial cells, immune cells, fibroblasts, and vascular endothelial cells, for their potential to model RSV infection and support pharmaceutical research. RSV-infected organoids exhibited high viral genome and protein expression, epithelial layer destruction, and increased collagen accumulation. Pro-inflammatory cytokine levels in culture supernatants also increased post-infection. Furthermore, RSV infection was significantly inhibited by monoclonal antibodies (nirsevimab, palivizumab, suptavumab, or clesrovimab), while ribavirin showed limited efficacy. These findings highlight the utility of respiratory organoids for RSV research.
2025-04-21 | GSE263272 | GEO
Project description:Respiratory syncytial virus (RSV) is a seasonal respiratory pathogen that primarily affects young children, potentially causing severe lower respiratory tract disease. Despite the high disease burden, understanding of RSV pathophysiology remains limited. To address this, advanced RSV infection models are needed. While HEp-2 cells are widely used due to their high susceptibility to RSV, they do not accurately reflect the host response of the human respiratory tract. In this study, we evaluated human induced pluripotent stem cell-derived respiratory organoids, which contain respiratory epithelial cells, immune cells, fibroblasts, and vascular endothelial cells, for their potential to model RSV infection and support pharmaceutical research. RSV-infected organoids exhibited high viral genome and protein expression, epithelial layer destruction, and increased collagen accumulation. Pro-inflammatory cytokine levels in culture supernatants also increased post-infection. Furthermore, RSV infection was significantly inhibited by monoclonal antibodies (nirsevimab, palivizumab, suptavumab, or clesrovimab), while ribavirin showed limited efficacy. These findings highlight the utility of respiratory organoids for RSV research.
2025-04-21 | GSE263271 | GEO
Project description:Respiratory syncytial virus (RSV) is a seasonal respiratory pathogen that primarily affects young children, potentially causing severe lower respiratory tract disease. Despite the high disease burden, understanding of RSV pathophysiology remains limited. To address this, advanced RSV infection models are needed. While HEp-2 cells are widely used due to their high susceptibility to RSV, they do not accurately reflect the host response of the human respiratory tract. In this study, we evaluated human induced pluripotent stem cell-derived respiratory organoids, which contain respiratory epithelial cells, immune cells, fibroblasts, and vascular endothelial cells, for their potential to model RSV infection and support pharmaceutical research. RSV-infected organoids exhibited high viral genome and protein expression, epithelial layer destruction, and increased collagen accumulation. Pro-inflammatory cytokine levels in culture supernatants also increased post-infection. Furthermore, RSV infection was significantly inhibited by monoclonal antibodies (nirsevimab, palivizumab, suptavumab, or clesrovimab), while ribavirin showed limited efficacy. These findings highlight the utility of respiratory organoids for RSV research.
2025-04-21 | GSE260752 | GEO
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
Project description:we examine the effect of RSV infection in human small airway epithelial cells (hSAECs)
2021-02-26 | GSE167486 | GEO
Project description:Respiratory Syncytial virus (RSV)
| PRJNA973580 | ENA