Ontology highlight
ABSTRACT:
PROVIDER: PRJNA750472 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15289051.fastq.gz | Fastqsanger.gz | |||
| SRR15289052.fastq.gz | Fastqsanger.gz | |||
| SRR15289053.fastq.gz | Fastqsanger.gz | |||
| SRR15289054.fastq.gz | Fastqsanger.gz | |||
| SRR15289055.fastq.gz | Fastqsanger.gz |
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Project description:Marburg virus is a genetically simple RNA virus that causes a severe hemorrhagic fever upon infection in humans and non-human primates. The mechanism of how this pathogenesis comes about is not well understood, but it is well accepted that pathogenesis is significantly driven by a hyperactive immune response. To better understand the overall response to Marburg virus challenge, we undertook a transcriptomic analysis of immune cells circulating in the blood following aerosol exposure of cynomolgus macaques to a lethal dose of Marburg virus. Using two-color microarrays, we analyzed the transcriptome of peripheral blood mononuclear cells that were collected throughout the course of infection from 1 to 9 days postexposure, representing the full course of the infection. The host response to aerosolized Marburg was evident at 1 day post-exposure. The response followed a 3-phase response that was led by a robust innate immune response. Analysis of cytokine transcripts that were overexpressed during infection indicated that previously unanalyzed cytokines are likely induced in response to exposure to Marburg virus, and further suggested that the immune response may favor a Th2 response that would hamper the development of an effective antiviral immune response. Late infection events included the upregulation of coagulation associated factors. These findings suggest new avenues for investigating the pathogenesis of Marburg virus infection and provide rich dataset of factors expressed throughout the course of infection that can be investigated as markers of infection and targets for therapy. RNA was isolated from a total of 30 PBMC samples from 15 cynomologus macaques infected with Marburg Virus. Samples were obtained at sequential timepoints post-infection, and included a pre-infection specimen from each animal. These samples were then processed and hybridized onto the Agilent 2-color arrays.
2015-05-11 | E-GEOD-58287 | biostudies-arrayexpress
Project description:Marburg virus is a genetically simple RNA virus that causes a severe hemorrhagic fever upon infection in humans and non-human primates. The mechanism of how this pathogenesis comes about is not well understood, but it is well accepted that pathogenesis is significantly driven by a hyperactive immune response. To better understand the overall response to Marburg virus challenge, we undertook a transcriptomic analysis of immune cells circulating in the blood following aerosol exposure of cynomolgus macaques to a lethal dose of Marburg virus. Using two-color microarrays, we analyzed the transcriptome of peripheral blood mononuclear cells that were collected throughout the course of infection from 1 to 9 days postexposure, representing the full course of the infection. The host response to aerosolized Marburg was evident at 1 day post-exposure. The response followed a 3-phase response that was led by a robust innate immune response. Analysis of cytokine transcripts that were overexpressed during infection indicated that previously unanalyzed cytokines are likely induced in response to exposure to Marburg virus, and further suggested that the immune response may favor a Th2 response that would hamper the development of an effective antiviral immune response. Late infection events included the upregulation of coagulation associated factors. These findings suggest new avenues for investigating the pathogenesis of Marburg virus infection and provide rich dataset of factors expressed throughout the course of infection that can be investigated as markers of infection and targets for therapy.
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Project description:Microarray data was used to study the gene expression changes following dengue infection at various time points to identify host genes and pathways responsible for dengue virus replication Keywords: time course
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Project description:Microarray data was used to study the gene expression changes following dengue infection at various time points to identify host genes and pathways responsible for dengue virus replication Keywords: time course
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Project description:Marburg virus, a member of the Filoviridae, is the causative agent of Marburg virus disease (MVD), a hemorrhagic fever with a case fatality rate of up to 90%. Acute kidney injury is common in MVD and is associated with increased mortality, but its pathogenesis in MVD remains poorly understood. Interestingly, autopsies show the presence of viral proteins in different parts of the nephron, particularly in proximal tubular cells (PTC). These findings suggest a potential role for the virus in the development of MVD-related kidney injury. To shed light on this effect, we infected primary human PTC with Lake Victoria Marburg virus and conducted transcriptomic analysis at multiple time points. Unexpectedly, infection did not induce marked cytopathic effects in primary tubular cells at 20 and 40 hours post infection. However, gene expression analysis revealed robust renal viral replication and dysregulation of genes essential for different cellular functions. The gene sets mainly downregulated in PTC were associated with the targets of the transcription factors MYC and E2F, DNA repair, the G2M checkpoint, as well as oxidative phosphorylation. Importantly, the downregulated factors comprise PGC-1α, a well-known factor in acute and chronic kidney injury. By contrast, the most highly upregulated gene sets were those related to the inflammatory response and cholesterol homeostasis. In conclusion, Marburg virus infects and replicates in human primary PTC and induces downregulation of processes known to be relevant for acute kidney injury as well as a strong inflammatory response.
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Project description:The host response to influenza A infections is strongly influenced by host genetic factors. Animal models of genetically diverse mouse strains are well suitable to identify host genes involved in severe pathology, viral replication and immune responses. Here, we have utilizing a dual RNAseq approach that allowed us to investigate both viral and host gene expression in the same individual from a single expression assay after H1N1 infection. We performed a comparative expression analysis to identify (i) correlations between host genes and the viral gene expression, (ii) host genes involved in viral replication, and (iii) genes showing differential expression between the two mouse strains after infection. These genes may be key players involved in regulating the differences in pathogenesis and host defense mechanisms after influenza A infections. Expression levels of influenza segments correlated well with the viral load and may thus be used as surrogates for conventional viral load measurements. Furthermore, we investigated the functional role of two genes, Reg3g and Irf7, in knock-out mice and found that deletion of the Irf7 gene renders the host highly susceptible to H1N1 infection. Female, 10-12 weeks old mice were anesthetized by intra-peritoneal injection with Ketamine/Xylazine (85% NaCl (0.9%), 10% Ketamine, 5% Xylazine) with doses adjusted to the individual body weight. Mice were then intra-nasally infected with 20µl virus solution (2x10³ FFU PR8M) or mock-treated with PBS.
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