Transcriptome Responses of the Host Spodoptera litura upon Spodoptera litura nucleopolyhedrovirus infection
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ABSTRACT:
ORGANISM(S): Spodoptera litura
PROVIDER: GSE68037 | GEO | 2015/04/22
SECONDARY ACCESSION(S): PRJNA281733
REPOSITORIES: GEO
Similar Datasets
Project description:To reveal dynamic regulation of host gene expression and an overview of events in the infection cycle after SpltNPV infection To analyze cellular responses to SpltNPV infection, a S.litura cell line (SL221) was infected with wild-type baculovirus SpltNPV at a MOI of 1. RNAs were isolated at three time points through the infection cycle (6hpi, 12hpi and 18hpi) and also from control (mock infected) cells. The obtained cellular ranscriptome from the host S.litura was set for illumina strand specific RNA sequencing (RNA-seq) to analyze changes in host cell gene expression upon SpltNPV infection.
2015-04-22 | E-GEOD-68037 | biostudies-arrayexpress
Project description:Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV) is the best-studied baculovirus and most commonly used virus vector for baculovirus expression vector systems. The effect of AcMNPV infection on host cells is incompletely understood. A microarray based on Spodoptera frugiperda ESTs was used to investigate the impact of AcMNPV on host gene expression in cultured S. frugiperda, Sf21 cells. Most host genes were down-regulated over the time course of infection, although a small number were up-regulated. The most highly up-regulated genes encoded heat shock protein 70s and several poorly characterized proteins. Regulated genes with the highest score identified by functional annotation clustering included primarily products required for protein expression and trafficking in the ER and golgi. All were significantly down-regulated by approximately 12h post-infection. Microarray data were validated by qRT-PCR. This study provides the first comprehensive host transcriptome overview of Sf21 cells during AcMNPV infection.
2014-08-26 | GSE60739 | GEO
Project description:Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV) is the best-studied baculovirus and most commonly used virus vector for baculovirus expression vector systems. The effect of AcMNPV infection on host cells is incompletely understood. A microarray based on Spodoptera frugiperda ESTs was used to investigate the impact of AcMNPV on host gene expression in cultured S. frugiperda, Sf21 cells. Most host genes were down-regulated over the time course of infection, although a small number were up-regulated. The most highly up-regulated genes encoded heat shock protein 70s and several poorly characterized proteins. Regulated genes with the highest score identified by functional annotation clustering included primarily products required for protein expression and trafficking in the ER and golgi. All were significantly down-regulated by approximately 12h post-infection. Microarray data were validated by qRT-PCR. This study provides the first comprehensive host transcriptome overview of Sf21 cells during AcMNPV infection. Host gene expression of the Sf21 cells was measured in AcMNPV mock-infected Sf21cells as well as AcMNPV-infected Sf21 cells at 6, 12, and 24 hours post infection (hpi). Four independent experiments were performed at each time (6, 12, and 24 hpi) using different donors for each experiment. Only two 24 hour sample data sets were used in the final analysis as two did not meet QC criteria.
2014-08-26 | E-GEOD-60739 | biostudies-arrayexpress
Project description:We performed global host transcriptome analysis in human gingival epithelial cells upon Kaposi's sarcoma-associated herpesvirus (KSHV) infection to identify differentially expressed host genes. KSHV is a human oncogenic virus, which establishes persistent infection of the host. We collected mock as well as KSHV infected human gingival epithelial cells at 8 hours post-infection (hpi) in triplicate, and used the purified RNA for creating RNA-seq libraries for the analysis.
2023-01-25 | GSE223396 | GEO
Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another. The goal of this experiment was to use global gene expression profiling to understand swine lung host responses to pandemic H1N1 influenza A/Californica/04/2009 (CA04) virus infection and compare acute host responses across independent species. Four-week-old crossbred pigs (Sus Scrofa) were inoculated intratracheally with either 10^6 TCID50/pig egg-derived 2009 pandemic influenza A/California/04/2009 virus (n = 5) or mock inoculated with non-infectious cell culture supernatant (control; n = 4). Animals were euthanized on day 7 post-infection and lung samples were used for microarray.
2012-09-12 | E-GEOD-40847 | biostudies-arrayexpress
Project description:M. hominis adherence, colonisation and invasion of HeLa cells were characterised in a time-course study using microarray-based analysis of the HeLa cell transcriptome: 0 h to monitor the baseline of transcription, 4 h to examine host reactions to mycoplasma attachment, 48 h to capture in addition the initiation of invasion, and 2 weeks post infection to examine a chronically infected host cell. At 4 h post infection, cytoadherence of M. hominis to the HeLa cell surface was accompanied by differential regulation of 723 host genes (>2 fold change in expression). Genes associated with immune responses and signal transduction pathways were mainly affected and components involved in cell-cycle regulation, growth and death were highly upregulated. At 48 h post infection, when mycoplasma invasion started, 1588 host genes were differentially expressed and expression of genes for lysosome-specific proteins associated with bacterial lysis was detected. In a chronically infected HeLa cell line (2 weeks), of the 1972 regulated host genes, components of the ECM-receptor interaction pathway and phagosome-related integrins were markedly increased. The immune response was quite different to that at the beginning of infection, with a prominent induction of IL1B gene expression, affecting pathways of MAPK signalling, and genes connected with cytokine-cytokine interactions and apoptosis. These data show for the first time the complex, time-dependent reaction of the host directed at mycoplasmal clearance and the counter measures of this pestering pathogen. To elucidate the host-reactions at the different stages of M. hominis infection, four time points post infection (0h, 4h, 48h, 2 weeks) were chosen for microarray gene expression analyses. Total RNA was prepared from infection assays (MOI 100) in parallel with uninfected HeLa cells and the host cell transcriptomes were determined by comparative microarray analyses.
2014-02-06 | E-GEOD-54698 | biostudies-arrayexpress
Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another.
2012-09-12 | GSE40847 | GEO
Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another.
2012-08-14 | GSE40091 | GEO
Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another.
2012-08-14 | GSE40088 | GEO
Project description:Purpose: We analyzed the 3rd-instar Spodoptera frugiperda response after SfAV-1a infection. Specifically, we targeted three gene types in the infected host namely, mitochondrial, cytoskeleton and innate immunity genes.
2020-02-09 | GSE114901 | GEO