Lung response to Respiratory Syncytial Virus Infection in Adult and Old Mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE111947 | GEO | 2018/11/12
REPOSITORIES: GEO
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Project description:Transcriptional responses in lungs of mice infected with Respiratory Syncytial Virus (RSV) were compared to a control and mock infections
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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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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.
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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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