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Respiratory Syncytial virus (RSV) directly binds host microRNAs to de-regulate host gene targets [RNA-seq miR-27 over-expression]

ABSTRACT: Respiratory Syncytial virus (RSV) directly binds host microRNAs to de-regulate host gene targets [RNA-seq miR-27 over-expression]

PROVIDER: PRJNA967684 | ENA |

REPOSITORIES: ENA

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Respiratory Syncytial virus (RSV) directly binds host microRNAs and de-regulates host gene targets [miRNA-seq]

Project description:Respiratory Syncytial virus (RSV) directly binds host microRNAs and de-regulates host gene targets [miRNA-seq]

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Respiratory Syncytial virus (RSV) directly binds host microRNAs and de-regulates host gene targets [RNA-seq]

Project description:Respiratory Syncytial virus (RSV) directly binds host microRNAs and de-regulates host gene targets [RNA-seq]

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Respiratory Syncytial virus (RSV) directly binds host microRNAs and de-regulates host gene targets [RNA-seq]

Project description:To investigate RNA expression changes in RSV infection, we performed total RNA-seq from Mock and RSV-infected A549 cells In addition, we investigated the association of RNAs with AGO2 by performing AGO2 immunoprecipitation and total RNA-seq of AGO2-bound RNAs in Mock and RSV-infected A549 cells

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Respiratory Syncytial virus (RSV) directly binds host microRNAs and de-regulates host gene targets [miRNA-seq]

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Multi-organ profiles of C fiber degenerated (KPCF) mice and respiratory syncytial virus (RSV)-infected KPCF mice

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.

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Transcription profiling of lung and bronchial lymph node from mice infected with Respiratory Syncytial Virus (RSV)

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

Multi-organ profiles of respiratory syncytial virus (RSV)-infected BALB/c mice

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.

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Nasopharyngeal microbiota, host transcriptome and disease severity in children with respiratory syncytial virus infection

Project description:Rationale: Respiratory syncytial virus (RSV) is the leading cause of acute lower respiratory tract infections and hospitalizations in infants worldwide. Known risk factors, however, incompletely explain the variability of RSV disease severity among children. We postulate that severity of RSV infection is influenced in part by modulation of the host immune response by the local microbial ecosystem at the time of infection. Objectives: To define whether different nasopharyngeal microbiota profiles are associated with distinct host transcriptome profiles and severity in children with RSV infection. Methods: We analyzed the nasopharyngeal microbiota profiles of young children with mild and severe RSV disease and healthy matched controls by 16S-rRNA sequencing. In parallel, we analyzed whole blood gene expression profiles to study the relationship between microbial community composition, the RSV-induced host transcriptional response and clinical disease severity. Measurements and Main results: We identified five nasopharyngeal microbiota profiles characterized by enrichment of H. influenzae, Streptococcus, Corynebacterium, Moraxella or S. aureus. RSV infection and RSV hospitalization were positively associated with H. influenzae and Streptococcus, and negatively associated with S. aureus abundance, independent of age. The host response to RSV was defined by overexpression of interferon-related genes, and this was independent of the microbiota composition. On the other hand, transcriptome profiles of RSV infected children with H. influenzae and Streptococcus-dominated microbiota were characterized by greater overexpression of genes linked to toll-like receptor-signaling and neutrophil activation and were more frequently hospitalized Conclusions: Our data suggest an immunomodulatory role for the resident nasopharyngeal microbial community early in RSV infection, potentially affecting RSV disease severity.

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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.

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