Host-pathogen interactions in human polyomavirus 7 (HPyV7)-associated skin disease
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PROVIDER: PRJNA623371 | ENA |
REPOSITORIES: ENA
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Project description:The recently discovered polyomavirus HPyV7 is emerging as a cause for intensely itchy skin eruptions in immunocompromised hosts. We performed an in-depth investigation of a renal transplant recipient with HPyV7-associated eruption that resolved with reduction of immunosuppression and treatment with acitretin. RNA sequencing of diseased skin revealed a strong interferon response that decreased upon clinical resolution, correlating with cessation of viral protein expression and seroconversion for HPyV7-specific antibodies. Sequencing of HPyV7 revealed a mutagenic hotspot within a previously undetected agnoprotein gene. The cytosine deaminases APOBEC3A and APOBEC3B were significantly upregulated in affected skin, and the observed viral sequence modifications were consistent with APOBEC activity, suggesting that it may play a role in viral evolution in diseased skin. Through this multi-omic approach, we confirm a pathogenic role for HPyV7, identify signature components of the host response, and highlight the complex interplay between the skin immune microenvironment and viral mutagenesis.
2020-04-07 | GSE148169 | GEO
Project description:Marek’s disease is a contagious lymphoproliferative disease of chickens and is a unique model of viral oncogenesis. Mapping changes or states over the course of infection for both host and pathogen would have the potential to generate important insights into dynamic host-pathogen interactions. Here we introduced 3’ end enriched RNA-seq as a novel method to study host-pathogen interactions in Marek’s disease virus challenged chicken embryo fibroblasts cells, which allowed accurate profiling of gene expression and alternative polyadenylation sites for host and pathogen simultaneously. We totally identified 476 differentially expressed genes and 437 APA switching genes in host, including switching in tandem 3’ UTRs and switching between coding region and 3’ UTR. Most of these genes were related to innate immunity, apoptosis and metabolism, but two sets of genes overlapped a little suggesting two complementary mechanisms for regulating gene expression during infection. In summary, our results gave a relatively comprehensive insight into dynamic host-pathogen interactions in gene transcription regulation during Marek’s disease virus infection and suggested that 3’ end enriched RNA-seq was a promising method to investigate global host-pathogen interactions.
2017-09-22 | GSE92567 | GEO
Project description:An ex-vivo human skin model was used to investigate the host skin response to M. sympodialis on oily (supplemented with oleic acid) and non-oily skin. Host-pathogen interactions were analysed by different molecular techniques including proteomics.
2021-09-09 | PXD018404 | Pride
Project description:To advance our understanding of cellular host-pathogen interactions, technologies that facilitate the co-capture of both host and pathogen spatial transcriptome information are needed. Here, we present an approach to simultaneously capture host and pathogen spatial gene expression information from the same formalin-fixed paraffin embedded (FFPE) tissue section using the spatial transcriptomics technology. We applied the method to COVID-19 patient lung samples and enabled the dual detection of human and SARS-CoV-2 transcriptomes at 55 µm resolution. We validated our spatial detection of SARS-CoV-2 and identified an average specificity of 94.92% in comparison to RNAScope and 82.20% in comparison to in situ sequencing (ISS). COVID-19 tissues showed an upregulation of host immune response, such as increased expression of inflammatory cytokines, lymphocyte and fibroblast markers. Our colocalization analysis revealed that SARS-CoV-2+ spots presented shifts in host RNA metabolism, autophagy, NFκB, and interferon response pathways. Future applications of our approach will enable new insights into host response to pathogen infection through the simultaneous, unbiased detection of two transcriptomes.
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Project description:Host-pathogen genetic interactions underlie tuberculosis susceptibility in genetically diverse mice
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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:The goal of this project is to understand the etiology and pathology of host-pathogen interaction using high-throughput cellular phenotyping. By combining the expertise in pathogen biology, informatics and stem cell biology across the institute, this project will use targeted genetic modification in mouse embryonic stem cells to identify functions of host genes in innate immunity. We will also explore the biology of mouse embryonic stem cells and their differentiation into immune competent cells. To this end we will generate homozygous and inducible knockout lines in mouse embryonic stem cells, which will be differentiated into immune competent cells, such as macrophages or dendritic cells. These will be subjected to a panel of immune challenge and stimulation assays to characterise the functions of the disrupted genes. To identify new functions for mammalian genes in innate immunity we will:\Generate a panel of homozygous inducible gene knockout mouse ES cell lines working from a list of ca. 80 candidate genes (MGP phenotyping and GWAS hits). \Scale up differentiation protocols for immune challenge and stimulation assays.\Benchmark in vitro differentiated ES cell models against primary immune cells from selected MGP mouse lines and eventually against human iPS cells.\Screen a panel of 30 genetically modified cell lines in immunological challenge and stimulation assays, defining phenotypes at the cellular level by high content imaging, biochemically by assaying cytokine production, and at the molecular level by transcriptome analysis.\Define novel gene functions in innate immunity through network analysis of gene expression data from all challenged cell lines.\In the longer term scale up the production and phenotyping of genetically modified cell lines (mouse or human as appropriate).This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2014-03-25 | E-ERAD-234 | biostudies-arrayexpress
Project description:The outcome of an encounter with Mycobacterium tuberculosis (Mtb) depends on the pathogen’s ability to adapt to the heterogeneous immune response of the host. Understanding this interplay has proven difficult, largely because experimentally tractable small animal models do not recapitulate the heterogenous disease observed in natural infections. We leveraged the genetically diverse Collaborative Cross (CC) mouse panel in conjunction with a library of Mtb mutants to associate bacterial genetic requirements with host genetics and immunity. We report that CC strains vary dramatically in their susceptibility to infection and represent reproducible models of qualitatively distinct immune states. Global analysis of Mtb mutant fitness across the CC panel revealed that a large fraction of the pathogen’s genome is necessary for adaptation to specific host microenvironments. Both immunological and bacterial traits were associated with genetic variants distributed across the mouse genome, elucidating the complex genetic landscape that underlies host-pathogen interactions in a diverse population.
2021-01-04 | GSE164156 | GEO
Project description:The opportunistic fungal pathogen Candida albicans is a common cause of life-threatening nosocomial bloodstream infections. In the murine model of systemic candidiasis the kidney is the primary target organ while the fungal load declines over time in liver and spleen. To get a better understanding of the organ-specific differences in host-pathogen interaction during systemic murine candidiasis, we performed a time-course gene expression profiling to investigate the differential responses of murine kidney, liver and spleen and determined the fungal transcriptome in liver and kidney. We clearly demonstrate a delayed immune response on the transcriptional level in kidney accompanied by late induction of fungal stress response genes in this organ. In contrast, early upregulation of the proinflammatory response in the liver was associated with a fungal transcriptional profile resembling that of phagocytosed cells, suggesting that the resident phagocytic system contributes significantly to fungal control in the liver. Although no visible filamentation occurred in the liver, C. albicans hypha-associated genes were upregulated, indicating an uncoupling of gene expression and morphology during infection of this organ. In vitro the induction of hypha-associated gene expression in yeast cells led to altered interaction with macrophages, suggesting that the observed transcriptional changes affect host-pathogen interaction in vivo. Consistently, the combination of host and pathogen transcriptional data in an inference network model implied that C. albicans cell wall remodeling and metabolism were connected to the immune responses in kidney and liver. Furthermore, the network suggested links between fungal iron acquisition and amino acid metabolism in the kidney and host organ homeostasis. Thus, this work provides novel insights into the organ-specific host-pathogen interactions during systemic C. albicans infection.
2016-11-18 | GSE83679 | GEO
Project description:Strawberry is economically important and widely grown but susceptible to a large variety of phytopathogenic organisms. Among them, Xanthomonas fragariae is a quarantine bacterial pathogen threatening strawberry productions by causing angular leaf spots. Using whole transcriptome sequencing, gene expression of both plant and bacteria in planta was analyzed at two time points, 12- and 29-days post inoculation, in order to compare pathogen and host response between the stages of early visible and of well-developed symptoms. Among 28’588 known genes in strawberry and 4’046 known genes in X. fragariae expressed at both time points, a total of 361 plant and 144 bacterial genes were significantly differentially expressed, respectively. The identified higher expressed genes in the plants were pathogen-associated molecular pattern receptors and pathogenesis related thaumatin encoding genes, whereas the more expressed early genes were related to chloroplast metabolism as well as photosynthesis related coding genes. Most of X. fragariae genes involved in host interactions, recognitions and pathogenesis, were lower expressed at late-phase infection. This study gives a first insight on the interaction of X. fragariae with its host. The strawberry plant changed its metabolism consistently with the progression of infection.
2020-08-25 | GSE150636 | GEO