Respiratory syncytial virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1251136 | ENA |
REPOSITORIES: ENA
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Project description:Respiratory viral coinfections pose a substantial global health burden, yet the underlying virus–virus interactions remain incompletely understood. Here, we systematically examined the interplay among influenza A virus (IAV), SARS-CoV-2, and respiratory syncytial virus (RSV) using a reconstituted human airway epithelium model. We monitored viral replication dynamics and host transcriptional responses under both simultaneous and sequential infection conditions.
2026-01-30 | E-MTAB-16265 | biostudies-arrayexpress
Project description:We previously reported widespread differential expression of long non-protein-coding RNAs (ncRNAs) in response to virus infection. Here, we expanded the study through small RNA transcriptome sequencing analysis of the host response to both severe acute respiratory syndrome coronavirus (SARS-CoV) and influenza virus infections across four founder mouse strains of the Collaborative Cross, a recombinant inbred mouse resource for mapping complex traits. We observed differential expression of over 200 small RNAs of diverse classes during infection. A majority of identified microRNAs (miRNAs) showed divergent changes in expression across mouse strains with respect to SARS-CoV and influenza virus infections and responded differently to a highly pathogenic reconstructed 1918 virus compared to a minimally pathogenic seasonal influenza virus isolate. Novel insights into miRNA expression changes, including the association with pathogenic outcomes and large differences between in vivo and in vitro experimental systems, were further elucidated by a survey of selected miRNAs across diverse virus infections. The small RNAs identified also included many non-miRNA small RNAs, such as small nucleolar RNAs (snoRNAs), in addition to nonannotated small RNAs. An integrative sequencing analysis of both small RNAs and long transcripts from the same samples showed that the results revealing differential expression of miRNAs during infection were largely due to transcriptional regulation and that the predicted miRNA-mRNA network could modulate global host responses to virus infection in a combinatorial fashion. These findings represent the first integrated sequencing analysis of the response of host small RNAs to virus infection and show that small RNAs are an integrated component of complex networks involved in regulating the host response to infection. IMPORTANCE: Most studies examining the host transcriptional response to infection focus only on protein-coding genes. However, mammalian genomes transcribe many short and long non-protein-coding RNAs (ncRNAs). With the advent of deepsequencing technologies, systematic transcriptome analysis of the host response, including analysis of ncRNAs of different sizes, is now possible. Using this approach, we recently discovered widespread differential expression of host long (>200 nucleotide[nt]) ncRNAs in response to virus infection. Here, the samples described in the previous report were again used, but we sequenced another fraction of the transcriptome to study very short (about 20 to 30 nt) ncRNAs. We demonstrated that virus infection also altered expression of many short ncRNAs of diverse classes. Putting the results of the two studies together, we show that small RNAs may also play an important role in regulating the host response to virus infection. The small RNA transcriptome deep sequencing analysis was performed on lung samples from our previously published study (Unique signatures of long noncoding RNA expression in response to virus infection and altered innate immune signaling , X Peng, MBio. 2010 Oct 26;1(5). pii: e00206-10.). We infected four of the eight founder mouse strains used in generating the Collaborative Cross, a recombinant inbred mouse resource for mapping complex traits (41). These strains included 129S1/SvImJ (129/S1), WSB/EiJ (WSB), PWK/PhJ (PWK), and CAST/EiJ (CAST) mice. Ten-week-old mice were intranasally infected with phosphate-buffered saline (PBS) alone or with 1X10^5 PFU of mouse adapted severe acute respiratory syndrome coronavirus (SARS-CoV; rMA15), or 500 PFU of influenza A virus strain A/Pr/8/34 (H1N1; PR8). To match the previous whole-transcriptome analysis, we performed small RNA transcriptome sequencing analysis on the same eight samples from mice with SARS-CoV infections, including one SARS-CoV rMA15-infected mouse and one matched mock-infected mouse from each of the four strains at 2 days postinfection (dpi). In addition, we sequenced the small RNA transcriptome for 12 samples obtained from influenza virus infected mice, including two PR8-infected mice and one matched mockinfected mouse from each of the four strains at 2 dpi.
2012-03-31 | E-GEOD-36971 | biostudies-arrayexpress
Project description:The respiratory viruses can concurrently or sequentially infect a host and influence the trajectory of each other. The underlying immune mechanisms are not well understood. Here, we investigated whether respiratory syncytial virus (RSV) infection affects host vulnerability to subsequent SARS-CoV-2 infection in both BALB/c and the K18 hACE-2 transgenic mouse models. We found that RSV infection- induced heterologous protection against subsequent SARS-CoV-2 infection was dose and time dependent. RNA-seq and immunological analyses revealed that RSV infection triggered antigen presenting cell (APC)s and SARS-CoV-2 reactive mucosal T cell activation in the lung at day 9, which declined at 1 month. RSV infection induced the expansion and the upregulation of cellular metabolic pathways of gd T cells. Furthermore, RSV infection in TCRd-/- mice, which are deficient of gd T cells triggered a lower SARS-CoV-2 reactive mucosal T cell response. Following SARS-CoV-2 infection, TCRd-/- mice with prior RSV infection had increased viral loads and higher levels of virus-induced inflammatory responses in the lung compared to the WT group. In summary, our results suggest that RSV infection provides heterologous protection against subsequent SARS-CoV-2 infection via induction gd T cell- mediated trained immunity in the lung and SARS-CoV-2 reactive mucosal T cell responses.
2026-02-09 | GSE300910 | GEO
Project description:Respiratory syncytial virus Genome sequencing and assembly
| PRJNA438443 | ENA
Project description:Respiratory syncytial virus Genome sequencing and assembly
| PRJNA1369004 | ENA
Project description:Respiratory syncytial virus Genome sequencing and assembly
| PRJNA1419834 | ENA
Project description:Respiratory Syncytial Virus (RSV), alongside other prominent respiratory RNA viruses such as influenza and SARS-CoV-2, significantly contributes to the global incidence of respiratory tract infections. These pathogens prompt the production of reactive oxygen species (ROS), which play a crucial role in the onset and progression of respiratory diseases. However, the strategies by which viral RNA manages ROS-induced base oxidation are not well understood. Here we uncover that 8-oxo-7,8-dihydroguanine (8-oxoGua) is not merely an incidental byproduct of ROS activity but serves as a strategic adaptation of RSV RNA during replication within host cells. Through RNA immunoprecipitation and next-generation sequencing, we discovered that 8-oxoguanine DNA glycosylase 1 (OGG1) binding sites are predominantly found in the RSV antigenome, especially within guanine-rich areas. Further investigation revealed that viral ribonucleoprotein complexes specifically hijack OGG1. Crucially, our findings show that inhibiting OGG1's ability to recognize 8-oxoGua leads to a substantial reduction in RSV progeny production. Our results underscore the viral replication machinery's adaptation to oxidative challenges, pointing to the inhibition of OGG1's reading function as a potential novel strategy for antiviral intervention.
2024-06-13 | GSE269769 | GEO
Project description:Respiratory syncytial virus (RSV), along with other prominent respiratory RNA viruses such as influenza and SARS-CoV-2, significantly contributes to the global incidence of respiratory tract infections. These pathogens induce the production of reactive oxygen species (ROS), which play a crucial role in the onset and progression of respiratory diseases. However, the mechanisms by which viral RNA manages ROS-induced base oxidation remain poorly understood. Here we reveal that 8-oxo-7,8-dihydroguanine (8-oxoGua) is not merely an incidental byproduct of ROS activity but serves as a strategic adaptation of RSV RNA to maintain genetic fidelity within host cells. Through 8-oxoguanine DNA glycosylase 1 (OGG1) immunoprecipitation and LC_MS/MS, we discovered that RSV nucleoprotein is a principal partner of OGG1. Further investigation revealed that viral ribonucleoprotein complexes specifically hijack OGG1. Importantly, inhibiting OGG1's ability to recognize 8-oxoGua significantly reduces RSV progeny production. Our results underscore the viral replication machinery's adaptation to oxidative challenges, suggesting that inhibiting OGG1's reading function could be a novel strategy for antiviral intervention.
2024-10-09 | PXD053262 | Pride
Project description:APHL Respiratory Syncytial Virus Genome sequencing and assembly
| PRJNA1425122 | ENA
Project description:Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and other respiratory viruses -Coronavirus OC43, Coronavirus 229E, Influenza A/H1N1, Influenza A/H3N2, Influenza B, Respiratory Syncytial Virus RSV A and RSV B - were analysed by bottom-up proteomics of viral cultures. High coverage of viral proteins was acheived after culturing in serum-free conditions when compared to cultures grown using standard conditions including 2% fetal bovine serum.
2022-10-13 | PXD028562 | Pride