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Transcriptional Profiling of the Immune Response to Marburg Infection

ABSTRACT: 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.

ORGANISM(S): Homo sapiens Macaca fascicularis

PROVIDER: GSE58287 | GEO | 2015/05/11

SECONDARY ACCESSION(S): PRJNA251894

REPOSITORIES: GEO

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Transcriptional Profiling of the Immune Response to Marburg Infection

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

Transcriptomics of Marburg virus-infected proximal tubular cells

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.

2024-02-14 | GSE226148 | GEO

Transcriptional Profiling of the Immune Response to Marburg Infection

Project description:Transcriptional Profiling of the Immune Response to Marburg Infection

| PRJNA251894 | ENA

Project description:Immune correlates of postexposure vaccine protection against Marburg virus

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Infection of RoNi cells with Sendai Cantell virus, MARV371bat virus, and VP35 mutant MARV371bat-R301A virus at MOI of 1.0

Project description:Study was performed in order to determine the scope of antiviral response of Rousettus aegyptiacus-derived fibroblasts to Sendai and Marburg virus infection. This study aids in understanding the function of the expanded immune repertoire of Rosettus aegyptiacus.

2018-11-01 | GSE117367 | GEO

Global changes of expression patterns of vaccinia virus infected lungs of C57BL/6 mice.

Project description:Vaccinia virus infection of mouse lungs produces a focal infection within the lung remaining at the large bronchi throughout the course of infection. Animals die of respiratory failure with little edema and few infiltrating immune cells. It is well established that poxviruses control the host immune system by encoding multiple host defense pathway antagonists. The goal of this study was to examine the local response to infection within the lung given that the virus controls the host immune response.

2010-08-22 | GSE23738 | GEO

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Project description:Methanothermobacter marburgensis str. Marburg genome sequencing project

| PRJNA40103 | ENA

Multiwalled carbon nanotube-induced pulmonary inflammatory and fibrotic responses and genomic changes following aspiration exposure in mice: A 1-year postexposure study.

Project description:Pulmonary exposure to multiwalled carbon nanotubes (MWCNT) induces an inflammatory and rapid fibrotic response, although the long-term signaling mechanisms are unknown. The aim of this study was to examine the effects of 1, 10, 40, or 80 µg MWCNT administered by pharyngeal aspiration on bronchoalveolar lavage (BAL) fluid for polymorphonuclear cell (PMN) infiltration, lactate dehydrogenase (LDH) activity, and lung histopathology for inflammatory and fibrotic responses in mouse lungs 1 mo, 6 mo, and 1 yr postexposure. Further, a 120-µg crocidolite asbestos group was incorporated as a positive control for comparative purposes. Results showed that MWCNT increased BAL fluid LDH activity and PMN infiltration in a dose-dependent manner at all three postexposure times. Asbestos exposure elevated LDH activity at all 3 postexposure times and PMN infiltration at 1 mo and 6 mo postexposure. Pathological changes in the lung, the presence of MWCNT or asbestos, and fibrosis were noted at 40 and 80 µg MWCNT and in asbestos-exposed mice at 1 yr postexposure. To determine potential signaling pathways involved with MWCNT-associated pathological changes in comparison to asbestos, up- and down-regulated gene expression was determined in lung tissue at 1 yr postexposure. Exposure to MWCNT tended to favor those pathways involved in immune responses, specifically T-cell responses, whereas exposure to asbestos tended to favor pathways involved in oxygen species production, electron transport, and cancer. Data indicate that MWCNT are biopersistent in the lung and induce inflammatory and fibrotic pathological alterations similar to those of crocidolite asbestos, but may reach these endpoints by different mechanisms.

2018-04-06 | GSE112780 | GEO

Marburg marburgvirus strain:Angola

Project description:Marburg marburgvirus strain:Angola Transcriptome or Gene expression

| PRJNA264121 | ENA

Marburg marburgvirus isolate:Angola

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| PRJNA320428 | ENA