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LncRNA NRAV promotes respiratory syncytial virus (RSV) replication by regulating vesicle transportation via targeting miR-509-3p/Rab5c axis

ABSTRACT: NRAV could act as a ceRNA in NRAV/miR-509-3p/Rab5c axis during RSV infection, thus promoting RSV vesicle transport and accelerating RSV entry.

ORGANISM(S): Homo sapiens

PROVIDER: GSE145371 | GEO | 2020/02/24

REPOSITORIES: GEO

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LncRNA NRAV promotes respiratory syncytial virus (RSV) replication by regulating vesicle transportation via targeting miR-509-3p/Rab5c axis

Project description:LncRNA NRAV promotes respiratory syncytial virus (RSV) replication by regulating vesicle transportation via targeting miR-509-3p/Rab5c axis

| PRJNA607024 | ENA

Respiratory Syncytial Virus (RSV) optimizes the translational landscape during infection

Project description:Viral infection often triggers eukaryotic initiator factor 2α (eIF2α) phosphorylation, leading to global 5’-cap-dependent translation inhibition. RSV encodes messenger RNAs (mRNAs) mimicking 5’-cap structures of host mRNAs and thus inhibition of cap-dependent translation initiation would likely also reduce viral translation. We confirmed that RSV limits widespread translation initiation inhibition and unexpectedly found that the fraction of ribosomes within polysomes increases during infection, indicating higher ribosome loading on mRNAs during infection. We found that AU-rich host transcripts that are less efficiently translated under normal conditions become more efficient at recruiting ribosomes, similar to RSV transcripts. Viral transcripts are transcribed in cytoplasmic inclusion bodies, where the viral AU-rich binding protein M2-1 has been shown to bind viral transcripts and shuttle them into the cytoplasm. We further demonstrated that M2-1 is found on polysomes, and that M2-1 might deliver host AU-rich transcripts for translation.

2024-09-03 | GSE268742 | GEO

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.

2022-04-24 | GSE197868 | GEO

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

2024-05-29 | GSE231788 | GEO

Transcription profiling of human bronchial epithelial cells treated with respiratory syncytial virus (RSV) for 4 and 24 hours

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. Experiment Overall Design: 4 controls (vehicle-treated for 4 hours) Experiment Overall Design: 4 RSV-treated for 4 hours Experiment Overall Design: 4 RSV-treated for 24 hours

2007-10-02 | E-GEOD-3397 | biostudies-arrayexpress

Respiratory syncytial virus (RSV) F subunit vaccine with adjuvants affect immunity in BALB/c mice

Project description:Purpers: To verify the effect of adjuvants (Alhydrogel, AS02, AS03) on immunity of BALB/c mice induced by RSV-F subunit vaccine at the level of gene expression. Methodes:Four groups ((1) RSV-F, (2) RSV-F + Alhydrogel, (3) RSV-F + AS02, and (4) RSV-F + AS03) were analyzed in the transcriptome sequencing experiment. On days 0 and 14, vaccines were administered intramuscularly into the thigh muscle. 14 days after the last vaccination, blood samples from three BALB/c mice in each group were collected. RNA degradation and contamination were assayed. Concentration were measured using a Qubit RNA Assay Kit and a Qubit 2.0 Fluorometer. RNA integrity was assessed using an RNA Nano 6000 Assay Kit and a Bioanalyzer 2100 system. 3 μg RNA per qualified sample was used as input material for RNA library preparation. Sequencing libraries were generated using a NEBNext Ultra RNA Library Prep Kit for Illumina (New England Biolabs, US), and unique index codes were added to each sample. Result: We obtained sample gene expression information. The subsequent differentially expressed gene GO and KEGG enrichment analysis result suggested that AS02 regulates immune balance by activating TLR-4 and promotes Th1-type immune responses.

2020-01-15 | GSE143617 | GEO

Olfactomedin 4 serves as a marker for disease severity in pediatric Respiratory Syncytial Virus (RSV) infection

Project description:Respiratory viral infections follow an unpredictable clinical course in young children ranging from a common cold to respiratory failure. The transition from mild to severe disease occurs rapidly and is difficult to predict. The pathophysiology underlying disease severity has remained elusive. There is an urgent need to better understand the immune response in this disease to come up with biomarkers that may aid clinical decision making. In a prospective study, flow cytometric and genome-wide gene expression analyses were performed on blood samples of 26 children with a diagnosis of severe, moderate or mild Respiratory Syncytial Virus (RSV) infection. Differentially expressed genes were validated using Q-PCR in a second cohort of 80 children during three consecutive winter seasons. FACS analyses were also performed in the second cohort and on recovery samples of severe cases in the first cohort. Severe RSV infection was associated with a transient but marked decrease in CD4+ T, CD8+ T, and NK cells in peripheral blood. Gene expression analyses in both cohorts identified Olfactomedin4 (OLFM4) as a fully discriminative marker between children with mild and severe RSV infection, giving a PAM cross-validation error of 0%. Patients with an OLFM4 gene expression level above -7.5 were 6 times more likely to develop severe disease, after correction for age at hospitalization and gestational age. In conclusion, by combining genome-wide expression profiling of blood cell subsets with clinically well-annotated samples, OLFM4 was identified as a biomarker for severity of pediatric RSV infection. Samples were taken of 26 patients with acute RSV infections, divided into mild (n=9), moderate (n=9) and severe (n=8) disease. From moderate and severe diseased patients recovery samples were obtained as well.

2015-06-06 | E-GEOD-69606 | biostudies-arrayexpress

Expression data from Toll-like receptor 4 (Tlr4)-deficient mice infected with respiratory syncytial virus (RSV)

Project description:In airway epithelial cells, Tlr4 mediates both innate and adaptive immune responses to viral pathogens through the surface fusion glycoprotein (RSV F), however the mechanism is not well characterized. We used microarrays to identify Tlr4-mediated gene expression pathways induced by RSV infection.

2019-08-28 | GSE111861 | GEO

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 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.

2022-10-11 | GSE215099 | GEO

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