Single-cell temporal characterization of RSV infection
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ABSTRACT:
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE281623 | GEO | 2025/04/16
REPOSITORIES: GEO
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Project description:Respiratory Syncytial virus (RSV) is the most common cause of childhood viral bronchiolitis and lung injury. Inflammatory responses significantly contribute to lung pathologies during RSV infections and bronchiolitis but the exact mechanisms have not been completely defined. The double-stranded RNA-activated protein kinase (PKR) functions to inhibit viral replication and participates in several signaling pathways associated with innate inflammatory immune responses. Using a functionally defective PKR (PKR-/-) mouse model, we investigated the role of this kinase in early events of RSV-induced inflammation. Our data showed that bronchoalveolar lavage (BAL) fluid of infected PKR-/- mice had significantly lower levels of several innate inflammatory cytokines and chemokines. Histological examinations revealed that there was less lung injury in infected PKR-/- mice as compared to the wild type. A genome-wide analysis showed that several early anti viral and immune regulatory genes were affected by PKR activation. These data suggest that PKR is a signaling molecule for immune responses during RSV infections.
2009-09-23 | GSE18170 | GEO
Project description:We studied RSV infection in an appropriate in vitro model of respiratory epithelium, a pseudostratified and fully differentiated mucociliary epithelium of normal human bronchial epithelial (NHBE) cells. RSV infection increased actin cytoskeleton without compromising adherent-, tight-, and tricellular-junctions as well as ciliary functions and epithelial tissue barrier integrity. This increased cytoskeleton depends on actin polymerization and the induction of proinflammatory cytokines and chemokines. Thus, we observed a novel signature “increased cytoskeleton” termed “cytoskeletal inflammation” in RSV-infected respiratory epithelium that presumably lacks classical antigen presenting cells, such as resident dendritic cells and macrophages. Our results suggest that RSV-induced cytoskeletal inflammation is a noncanonical earliest host response to the pathogen and contributes to airway inflammation.
2023-03-10 | GSE146795 | GEO
Project description:RSV, a leading cause of severe respiratory illnesses in vulnerable populations, lacks effective, affordable treatments for pediatric use. The potential of traditional Chinese medicine for relieving viral symptoms prompted this investigation into Xuanfei Formula (XFF) as an anti-RSV agent. This study employed H&E staining, cytokine profiling, and RSV titer quantification in BALB/c mice to evaluate the impact of XFF on RSV infection. Strikingly, immediate post-treatment observation showed a precipitous drop in both serum pro-inflammatory cytokine levels and pulmonary RSV-N gene copies in comparison to infected controls, suggesting XFF’s direct anti-RSV action. Transcriptome analyses were used to pinpointed the underlying mechanism behind formula’s immune-independent anti-RSV, a leading cause of severe respiratory illnesses in vulnerable populations, lacks effective, affordable treatments for pediatric use. The potential of traditional Chinese medicine for relieving viral symptoms prompted this investigation into Xuanfei Formula (XFF) as an anti-RSV agent. This study employed H&E staining, cytokine profiling, and RSV titer quantification in BALB/c mice to evaluate the impact of XFF on RSV infection. Strikingly, immediate post-treatment observation showed a precipitous drop in both serum pro-inflammatory cytokine levels and pulmonary RSV-N gene copies in comparison to infected controls, suggesting XFF’s direct anti-RSV action. Transcriptome analyses were used to pinpointed the underlying mechanism behind formula’s immune-independent anti-RSV effects during infection.
2024-04-25 | GSE263754 | GEO
Project description:The objective of this study was to identify gene expression markers of disease severity in a cohort of RSV infected children Respiratory syncytial virus (RSV) is the number one pathogen causing lower respiratory tract infection that leads to hospitalization in young children. Despite growing insights in the disease pathogenesis, the clinical presentation in these children is highly variable and heterogeneous, and reliable markers predictive of disease progression are lacking. We characterized the host response to acute RSV infection to identify biomarkers associated with RSV disease and disease severity. Whole genome transcriptome was analysed early on the disease course in blood samples from otherwise healthy children <2 years of age, who were either hospitalized (n = 110) or evaluated as outpatients (n = 37) due to RSV infection. Age-matched non-RSV-infected healthy children (n = 51) were analysed in parallel. A clustering approach on the transcriptome data revealed biologically meaningful biomarkers associated with progression to severe RSV disease. Overall, the whole blood transcriptome pointed to alterations in frequency of specific immune cell types (neutrophils, T- and B-lymphocytes, NK cells, monocytes) in RSV-infected children. In addition, a cluster enriched for neutrophil degranulation genes, was highly correlated with clinical disease severity. The driver genes of this cluster (OLFM4, ELANE, MMP8, BPI, CEACAM8, LCN2, LTF and MPO) were selected and validated in independent existing transcriptomics datasets. We identified a set of genes involved in neutrophil degranulation as markers for RSV disease severity. Additional prospective studies using these markers are required to further confirm their value as predictive tool in routine clinical care.
2022-01-21 | GSE188427 | GEO
Project description:mRNA expression data from BALB/c mice which were infected intranasally with Respiratory Syncytial Virus (or Hep-2 cell lysate control) at 1 week old and challenged with PBS or house dust mite (HDM) extract as adults. Experimental groups: RH – neonatal RSV, adult HDM, RP – neonatal RSV, adult PBS, HH – neonatal Hep-2, adult HDM and HP – neonatal Hep-2, adult PBS.
2019-03-19 | E-MTAB-3654 | biostudies-arrayexpress
Project description:RSV intra-host genetic diversity in adults during the epidemic of spring 2021, France
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Project description:A few transformed cell lines and two historic strains have been extensively used to study respiratory syncytial virus (RSV). We report a thorough molecular and cell biological characterization of HEp-2 and A549 cells infected with four strains of RSV representing both major subgroups as well as historic and more contemporary genotypes -- [RSV/A/Tracy (GA1), RSV/A/Ontario (ON), RSV/B/18537 (GB1), RSV/B/Buenos Aires (BA)] -- via measurements of viral replication kinetics and viral gene expression, immunofluorescence-based imaging of gross cellular morphology and cell-associated RSV, and measurements of host response including transcriptional changes and levels of secreted cytokines and growth factors. Our findings strongly suggest 1) the existence of a conserved difference in gene expression between RSV subgroups A and B; 2) the A549 cell line is a more stringent and natural host of replicating RSV than the HEp-2 cell line; and 3) consistent with previous studies, determining the full effects of viral genetic variation in RSV pathogenesis requires model systems as tractable as transformed cell lines but better representative of the human host.
2022-02-10 | GSE196385 | GEO
Project description:Respiratory syncytial virus (RSV) a leading cause of pediatric and adult morbidity and mortality worldwide. It can cause complications in multiple organs, thus increasing hospital stays and costs. However, RSV-based studies have primarily focused on effects in the lungs and blood, thereby potentially neglecting critical genes and pathways. Hence, studying RSV infection via a novel multi-organ approach is important. In this study, lung, intestine, brain, and spleen tissues from six BALB/c mice (6–8 weeks old; three in control group and three in RSV-infected group) were subjected to RNA sequencing. Differentially expressed genes (DEGs) in each organ were obtained and functional enrichment analysis was performed. We first used CIBERSORT to evaluate the immune-infiltration landscape. Subsequently, common DEGs (co-DEGs) among the four organs were analyzed to identify key genes and pathways. After quantitative reverse transcription-polymerase chain reaction, western blotting, and external validation analysis of key hub genes, their correlation with immune cells and potential functions were explored. We found that the host response to RSV infection varied among the four organs regarding gene expression profiles and immune cell infiltration. Analysis of the 16 co-DEGs indicated enrichment in the platelet and neutrophil degranulation pathways. Importantly, the key gene hemopexin (Hpx) was strongly correlated with the immune cell fraction in the lungs and may participate in the regulation of platelet activation and immune response.
2022-04-24 | GSE197868 | GEO
Project description:Despite being exposed to respiratory syncytial virus (RSV) infection multiple times in our lives, infants, older-adults, and immunocompromised patients are vulnerable to RSV-associated severe diseases, such as bronchiolitis and pneumonia. Respiratory viral infections are known to promote pulmonary fibrosis formation, which are often associated with a cellular remodeling process epithelial-mesenchymal transition (EMT). However, there is no information on whether RSV causes EMT in bronchial epithelial cells. Our results suggest that RSV-infection does not induce EMT in three different in vitro lung models: epithelial A549 cell line, primary normal human bronchial epithelial cells, and pseudostratified airway epithelium. Interestingly, RSV infection increased cell surface area and perimeter in the infected airway epithelium, which is distinct from the TGF-β1 driven cell elongation. Genome-wide transcriptome analysis also revealed that RSV infection is not involved in cell motility and locomotion. Thus, our results suggest that RSV infection does not induce EMT in the airway epithelium
2023-06-13 | GSE189537 | GEO
Project description:Rationale: Respiratory syncytial virus (RSV) and Streptococcus pneumoniae are major respiratory pathogens. Co-infection with RSV and S. pneumoniae is associated with severe and often fatal pneumonia but the molecular basis for this remains unclear. Objectives: To determine if interaction between RSV and pneumococci enhances pneumococcal virulence. Methods: We used confocal microscopy and western blot to identify the receptors involved in direct binding of RSV and pneumococci, the effects of which were studied in both in vivo and in vitro models of infection. Human ciliated respiratory epithelial cell cultures were infected with RSV for 72h and then challenged with pneumococci. Pneumococci were collected after 2h exposure and changes in gene expression determined using qRT-PCR. Results: Following incubation with RSV or purified G protein, pneumococci demonstrated a significant increase in the inflammatory response and bacterial adherence to human ciliated epithelial cultures and markedly increased virulence in a pneumonia model in mice. This was associated with extensive changes in the pneumococcal transcriptome and significant upregulation in the expression of key pneumococcal virulence genes, including the gene for the pneumococcal toxin, pneumolysin. We show that mechanistically this is due to RSV G glycoprotein binding penicillin binding protein 1a. Conclusion: The direct interaction between a respiratory virus protein and the pneumococcus resulting in increased bacterial virulence and worsening disease outcome is a new paradigm in respiratory infection. Comparison of the Streptococcus pneumoniae D39 RSV treated compared to BSA Treated in BEBM medium One condition design comparision of two strains including a dye swap
2014-06-21 | E-GEOD-58425 | biostudies-arrayexpress