Total Ribo depleted RNA-Seq of the supernatant across passages for the Metavac®-RSV mucosal bivalent vaccine candidate
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ABSTRACT:
PROVIDER: PRJEB86015 | ENA |
REPOSITORIES: ENA
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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
Project description:The aim of this investigation was two-fold: i) to describe miRNAs involved in the immune response to Respiratory syncytial virus (RSV) in a clinical setting in order to inform further research of immune system regulation by miRNAs in RSV or other infections; ii) to discover differences in miRNA expression between disease severity groups. We have therefore profiled miRNA in cytology brushings of the nasal mucosa in infants with RSV disease, comparing them to healthy infants. miRNA microarray identified 26 differentially regulated miRNA which were subsequently analyzed by RT-qPCR.
2014-10-15 | GSE62306 | 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: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.
2014-06-21 | GSE58425 | GEO
Project description:Human bronchial epithelial cells (BEAS-2B cells) were treated with RSV at 1.0 MOI for 4 and 24 hours or control (vehicle-treated for 4 hours). Global gene expression was measured by Affy Hu133 plus 2.0 microarray chips. Keywords: Inflammation, microtubules, RSV, time course
2006-05-01 | GSE3397 | 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: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: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.
2014-06-21 | GSE58424 | GEO
Project description:Although licensed vaccines against influenza virus have been successful in reducing pathogen-mediated disease, they have been less effective at preventing viral infection of the airways and current seasonal updates to influenza vaccines do not always successfully accommodate viral drift. Most licensed influenza and recently licensed RSV vaccines are administered via the intramuscular route. Alternative immunisation strategies, such as intranasal vaccinations, and "prime-pull" regimens, may deliver a more sterilising form of protection against respiratory viruses. A bivalent ChAdOx1-based vaccine (ChAdOx1-NP + M1-RSVF) encoding conserved nucleoprotein and matrix 1 proteins from influenza A virus and a modified pre-fusion stabilised RSV A F protein, was designed, developed and tested in preclinical animal models. The aim was to induce broad, cross-protective tissue-resident T cells against heterotypic influenza viruses and neutralising antibodies against RSV in the respiratory mucosa and systemically. When administered via an intramuscular prime-intranasal boost (IM-IN) regimen in mice, superior protection was generated against challenge with either RSV A, Influenza A H3N2 or H1N1. These results support further clinical development of a pan influenza & RSV vaccine administered in a prime-pull regimen.
| S-EPMC11208422 | biostudies-literature
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