Human respiratory syncytial virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA262901 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR7647880.fastq.gz | Fastqsanger.gz | |||
| SRR7647880_1.fastq.gz | Fastqsanger.gz | |||
| SRR7647880_2.fastq.gz | Fastqsanger.gz | |||
| SRR7647890.fastq.gz | Fastqsanger.gz |
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Project description:In this study we investigated whether there exists a genomic signature that can accurately predict the course of a respiratory syncytial virus (RSV) infection in hospitalized young infants. We used early blood microarray transcriptome profiles from 39 infants that were followed until recovery and of which the level of disease severity was determined retrospectively. Applying support vector machine learning on age by sex standardized transcriptomic data, an 84 gene signature was identified that discriminated hospitalized infants with eventually less severe RSV infection from infants that suffered from most severe RSV disease.
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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.
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Project description:N6-methyladenosine (m6A) is the most prevalent internal modification of mRNAs in most eukaryotes. Likewise, viral RNAs may acquire m6A methylation during replication within these cells. Here we show that RNAs of human respiratory syncytial virus (RSV), a medically important non-segmented negative-sense (NNS) RNA virus, are modified by m6A within discreet regions and that these modifications enhance viral replication and pathogenesis. Overexpression of m6A binding proteins significantly enhanced RSV replication and gene expression. Knockdown of m6A methyltransferases decreased viral replication and gene expression whereas knockdown of m6A demethylases had the opposite effect. The G gene contained the most abundant m6A modifications. Recombinant RSV expressing a G gene lacking different m6A sites, resulted in RSVs with various degrees of defects in replication in A549 cells, primary well differentiated human airway epithelial (HAE) cultures, upper and lower respiratory tract of cotton rats, and were also less pathogenic to the lungs of cotton rats. One of the m6A-deficient rgRSVs, rgRSV-G12, was completely attenuated yet retained high immunogenicity in cotton rats. Moreover, a small molecule that inhibits S-adenosyl-L-homocysteine (SAH) hydrolase, thereby reducing the cellular SAH pool and viral RNA m6A, also inhibited RSV replication in HAE cells. Collectively, our results demonstrate viral m6A methylation upregulates RSV replication and pathogenesis and identify viral m6A methylation as a target for rational design of live attenuated vaccine candidates and for novel antiviral therapeutic agents for RSV.
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