Gene expression profiling in the pathogenesis of Visna-Maedi viral disease
Ontology highlight
ABSTRACT:
ORGANISM(S): Ovis aries
PROVIDER: GSE107322 | GEO | 2020/11/23
REPOSITORIES: GEO
Similar Datasets
Project description:Using microarray technology, we aim to identify in vitro host gene expression for understanding the crosstalk of signaling pathways that leads to the joint pathogenesis in Avian orthoreovirus infection.
2018-05-09 | GSE103067 | GEO
Project description:We have used deep sequencing to follow polyomavirus infection of mouse NIH3T6 cells. We carried out RNA-seq at various times after infection and analyzed the host transcriptomes. Alignment of sequencing reads to the host genome showed that by late times in infection, 359 host transcripts were seen to be upregulated and 857 were downregulated more than 1.5 fold.
2015-05-29 | GSE69314 | GEO
Project description:Abstract: The COVID-19 (Coronavirus disease-2019) pandemic, caused by the SARS-CoV-2 coronavirus, has highlighted emergent viruses as significant threats to public health and the global economy. SARS-CoV-2 is closely related to the more lethal but less transmissible coronaviruses SARS-CoV-1 and MERS-CoV. Here, we have carried out comparative viral-human protein-protein interaction and viral protein localization analysis for all three viruses. We find that proteins often do not change localization across viruses but their sequence divergence dictates differences in host interactions. Functional genetic screening identified host factors that functionally impinge on coronavirus proliferation, including Tom70, a mitochondrial chaperone protein that interacts with both SARS-CoV-1 and SARS-CoV-2 Orf9b, an interaction we structurally characterized using cryoEM. Combining genetically validated host factors with both COVID-19 patient genetic data and medical billing records identified important molecular mechanisms (IL-17 regulation) and drug treatments (sigma-1 receptor ligands) that merit further molecular and clinical study.
2020-11-19 | MSV000086489 | MassIVE
Project description:Abstract: The COVID-19 (Coronavirus disease-2019) pandemic, caused by the SARS-CoV-2 coronavirus, has highlighted emergent viruses as significant threats to public health and the global economy. SARS-CoV-2 is closely related to the more lethal but less transmissible coronaviruses SARS-CoV-1 and MERS-CoV. Here, we have carried out comparative viral-human protein-protein interaction and viral protein localization analysis for all three viruses. We find that proteins often do not change localization across viruses but their sequence divergence dictates differences in host interactions. Functional genetic screening identified host factors that functionally impinge on coronavirus proliferation, including Tom70, a mitochondrial chaperone protein that interacts with both SARS-CoV-1 and SARS-CoV-2 Orf9b, an interaction we structurally characterized using cryoEM. Combining genetically validated host factors with both COVID-19 patient genetic data and medical billing records identified important molecular mechanisms (IL-17 regulation) and drug treatments (sigma-1 receptor ligands) that merit further molecular and clinical study.
2020-10-16 | PXD021588 | Pride
Project description:Competition and interplay between host and viral gene expression programs is a critical determinant of infection susceptibility and a potential target for anti-viral therapies. Viral infection is well documented to induce the expression of numerous host genes that are part of the innate immune response. Here we show that infection of human lung epithelial cells with Influenza A virus (IAV) also induces a broad program of alternative splicing of host genes. While these splicing-regulated genes are not enriched for known regulators of viral infection, we find that many of these genes do modulate the infection and/or replication of IAV in an siRNA screen. Moreover, inhibition of the IAV-induced splicing pattern in several genes tested also reduces viral infection. We further show that approximately a quarter of the IAV-induced splicing events are regulated by hnRNP K, a host protein we have previously implicated in the nuclear speckle-dependent splicing of the IAV M transcript. Notably, hnRNP K abundance at nuclear speckles is increased upon IAV infection. We propose that this change in subnuclear localization may alter the accessibility of hnRNP K for host transcripts, thereby leading to a program of host splicing changes that promote IAV replication.
2020-12-10 | GSE142499 | GEO
Project description:Alternaria brassicicola is a successful saprophyte and necrotrophic pathogen with a broad host range. It produces secondary metabolites that marginally affect virulence, in contrast to many A. alternata strains that produce secondary metabolites as host-specific pathogenicity factors. Cell wall-degrading enzymes (CWDEs) have been considered important for pathogenesis, but no CWDEs have been identified as significant virulence factors in A. brassicicola. In this study, we discovered mutants of a gene, AbVf19, which consistently produced smaller lesions than the wild type. The mutants grew slower than the wild type on an axenic medium with pectin as a major carbon source. Gene expression comparisons identified several hydrolytic enzyme-coding genes being down-regulated in the mutant during a late stage of infection. These down-regulated genes comprised a small fraction of genes within each family. Three of these genes had mutants that showed no or little change in virulence. This suggested that each down regulated gene only made a small contribution to virulence, or that their functions were redundant. This study demonstrated the existence and importance of a transcription factor that regulates a suite of genes that are probably important for decomposing and utilizing plant material during the late stage of plant infection. gene expression profile comparisons between wild type and a transcription factor mutant during host infection
2012-05-03 | E-GEOD-33148 | biostudies-arrayexpress
Project description:Background: Mycosis fungoides (MF), the most common cutaneous T-cell lymphoma, is often underdiagnosed in early stages due to similarities with benign dermatoses such as atopic dermatitis (AD). Furthermore, the delineation from so-called “parapsoriasis en plaque,” a disease that can appear either in a small- or large-plaque form, is still controversial. Here, we characterize the parapsoriasis disease spectrum. Methods: We performed single-cell RNA sequencing of skin biopsies from patients within the parapsoriasis-to-early-stage MF spectrum, stratified for small and large plaques, and compared them to AD, psoriasis and healthy control skin. Results: 6 out of 8 large-plaque lesions harbored either an expanded alpha/beta or gamma/delta T-cell clone with downregulation of CD7 expression, consistent with a diagnosis of early-stage MF. By contrast, 6 out of 7 small-plaque lesions were polyclonal in nature thereby lacking a lymphomatous phenotype, and also revealed a less inflammatory microenvironment than early-stage MF or AD. Of note, polyclonal small- and large-plaque lesions characteristically harbored a population of NPY+ innate lymphoid cells and displayed a stromal signature of complement upregulation and antimicrobial hyperresponsiveness in fibroblasts and sweat gland cells, respectively. These conditions were clearly distinct from AD or psoriasis, which uniquely harbored CD3+CRTH2+ IL13-expressing “Th2A” cells or strong type 17 inflammation, respectively. Conclusion: These data position polyclonal small- and large-plaque dermatitis lesions as a separate disease entity, that characteristically harbors a so far undescribed ILC population. We thus propose the new term “polyclonal parapsoriasis en plaque” to this kind of lesions, as they can be clearly differentiated from early and advanced-stage MF, psoriasis and AD on several cellular and molecular levels.
2024-10-24 | GSE247047 | GEO
Project description:<p>The overall purpose of this study is to investigate the host genetic factors in response to influenza virus infection, with the focus on influenza vaccination in the first substudy "Adult Influenza Vaccine Genetics" and with the focus on influenza natural infection and other acute respiratory infections (ARIs) in the second substudy "Acute Viral Respiratory Infection Genetics". In the first substudy, healthy adults were enrolled in 2008 (male cohort) and 2010 (female cohort) and immunized with seasonal influenza vaccine. In the second substudy, healthy adults were invited to enroll to be followed for acute respiratory illness through two consecutive influenza seasons 2009-2010 and 2010-2011. Peripheral blood genomic DNA samples were collected from all the subjects, and time-series RNA and serum samples were obtained pre- and post- immunization/infection. Genotyping was carried out on peripheral blood genomic DNA samples using Illumina HumanOmniExpress-12 v1 arrays. Peripheral blood RNA samples obtained at each visit were analyzed using Illumina Human HT-12 (for all the samples) and HiSeq 2000 (for 130 samples in the "Acute Viral Respiratory Infection Genetics" study). Serum specimens were tested using hemagglutination-inhibition (HAI) antibody assay for Influenza H1N1, H3N2, and Influenza B strains.</p> <p>A detailed description of each substudy is provided under their own pages below and via the grouping tool in the right-hand box: <ul> <li><a href="./study.cgi?study_id=phs000635">phs000635</a> Adult Influenza Vaccine Genetics</li> <li><a href="./study.cgi?study_id=phs001031">phs001031</a> Acute Viral Respiratory Infection Genetics</li> </ul> </p>
| phs001030 | dbGaP
Project description:The transcriptional profile of the porcine lung pathogen, Actinobacillus pleuropneumoniae, was monitored during the acute phase of infection in its natural host. Bacterial expression profiles of A. pleuropneumoniae isolated from lung lesions of 25 infected pigs were compared in samples taken 6, 12, 24 and 48 hours post infection.
2012-12-01 | GSE33999 | GEO
Project description:Infectious bursal disease virus (IBDV) is a highly contagious dsRNA virus (Birnaviridae) which causes immuno-suppression in chickens. Although largely controlled by vaccination, new, virulent strains of the virus mean that infectious bursal disease (IBD or ëGumboroí disease) still remains a threat to the poultry industry. The virus infects dividing IgM+ B-lymphocytes and the main site of viral replication is the bursa of Fabricius where B cells are produced. Infection is spread orally via contaminated feed and water. IBDV affects young birds, with the disease usually being diagnosed in 3-6 week old birds. Younger birds do not show clinical signs but are immuno-suppressed. Symptoms include anorexia, depression, diahorrea, ruffled feathers, immuno-suppression and bursal lesions. The disease peaks between 2-5 days post infection and is practically cleared by day 7. Mortality is variable but can be up to around 70% with very virulent strains of the disease. Even if birds survive, the resulting immuno-suppression and effect on egg production in layer birds is significant. Being able to breed commercial lines of birds for enhanced genetic resistance to IBDV is an obvious goal in the fight against the disease. Three-week-old chicks were inoculated with virus via an intra-nasal route and tissue samples were collected at 2, 3 and 4 days post-inoculation. Bursa and spleen tissues were examined from control and infected birds at 2, 3 and 4 days post-infection in birds known to be either susceptible or resistant to the virus. As well as understanding the host immune response to IBDV, we are interested in identifying genes involved in disease resistance and so we have analysed the gene expression profiles at these times, when the innate immune response is active. We assume that genes underlying resistance will be involved at this early stage of the host immune response.
2014-12-30 | E-TABM-1129 | biostudies-arrayexpress