WGS of HSV isolates
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB42849 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR5236850_1.fastq.gz | Fastqsanger.gz | |||
| ERR5236850_2.fastq.gz | Fastqsanger.gz | |||
| ERR5236731_1.fastq.gz | Fastqsanger.gz | |||
| ERR5236731_2.fastq.gz | Fastqsanger.gz | |||
| ERR5236833_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: To compare single cell transcriptional profiling (scRNAseq) of different murine genital herpes infection models with HSV1-McKrae and HSV2-186. Method: DMPA-treated WT C57BL/6 mice were infected with HSV1-McKrae, HSV2-186 or PBS intravaginally. Vaginal tissues were harvested at 5 days post infection, live cells were sorted, a minimum of 16,000 cells were used for scRNAseq. Results: By tSNE visualization of 21,633 cells across all samples, 17 distinct clusters were resolved. We found significantly increased levels of Interferons-Stimulated-Genes (ISGs) in the neutrophils potentially contributing to disease onset and progression in HSV2 genital infections. Conclusion: Our study is the first comparison between the transcriptional signature of two genital herpes model- namely HSV1 and HSV2. Generated by scRNAseq, this study would provide researchers with gene candidates associated with the disease progression and inflammation induced by genital infections with HSV1 and HSV2.
2020-12-31 | GSE161336 | GEO
Project description:This is an RNA-seq study of human lung transplant recipients. Bronchoalveolar lavage cells were collected on the first day after lung transplant. We performed bulk RNA-sequencing on 19 lung transplant recipients with severe primary graft dysfunction (PGD) and 19 lung transplant recipients without primary graft dysfunction. As this data is human identifiable, raw data are not included in this record.
2023-02-15 | E-MTAB-12282 | biostudies-arrayexpress
Project description:Using meta-analysis of eight independent transplant datasets (236 graft biopsy samples) from four organs, we identified a common rejection module (CRM) consisting of 11 genes that were significantly overexpressed in acute rejection (AR) across all transplanted organs. The CRM genes could diagnose AR with high specificity and sensitivity in three additional independent cohorts (794 samples). In another two independent cohorts (151 renal transplant biopsies), the CRM genes correlated with the extent of graft injury and predicted future injury to a graft using protocol biopsies. Inferred drug mechanisms from the literature suggested that two FDA-approved drugs (atorvastatin and dasatinib), approved for non-transplant indications, could regulate specific CRM genes and reduce the number of graft infiltrating cells during acute rejection. We treated mice with HLA-mismatched murine cardiac transplant with atorvastatin and dasatinib and showed reduction of the CRM genes, significant reduction of graft infiltrating cells, and extended graft survival. We further validated the beneficial effect of atorvastatina on graft survival by retrospective analysis of electronic medical records of a single-center cohort of 2,515 renal transplant patients. In conclusion, we identified a CRM in transplantation that provides new opportunities for diagnosis, drug repositioning and rational drug design. The eight transplant data sets used for discovery include GSE4315, GSE2596, GSE4470, GSE9377, GSE1563, GSE9493, GSE13440, GSE6095. The two additional independent cohorts of 151 transplant biopsies are GSE25902 and GSE1563. Not all samples from all studies were used. Only the samples marked as either AR or STA in each data set were used for analysis. The 101 samples in this study were used as case-control experiment between acute rejection (AR) and stable (STA) in renal transplant. The samples in this series are one of the three independent validation cohorts. The other two cohorts are described in GSE21374 and GSE36059
2013-10-04 | E-GEOD-50058 | biostudies-arrayexpress
Project description:Using meta-analysis of eight independent transplant datasets (236 graft biopsy samples) from four organs, we identified a common rejection module (CRM) consisting of 11 genes that were significantly overexpressed in acute rejection (AR) across all transplanted organs. The CRM genes could diagnose AR with high specificity and sensitivity in three additional independent cohorts (794 samples). In another two independent cohorts (151 renal transplant biopsies), the CRM genes correlated with the extent of graft injury and predicted future injury to a graft using protocol biopsies. Inferred drug mechanisms from the literature suggested that two FDA-approved drugs (atorvastatin and dasatinib), approved for non-transplant indications, could regulate specific CRM genes and reduce the number of graft infiltrating cells during acute rejection. We treated mice with HLA-mismatched murine cardiac transplant with atorvastatin and dasatinib and showed reduction of the CRM genes, significant reduction of graft infiltrating cells, and extended graft survival. We further validated the beneficial effect of atorvastatina on graft survival by retrospective analysis of electronic medical records of a single-center cohort of 2,515 renal transplant patients. In conclusion, we identified a CRM in transplantation that provides new opportunities for diagnosis, drug repositioning and rational drug design. The eight transplant data sets used for discovery include GSE4315, GSE2596, GSE4470, GSE9377, GSE1563, GSE9493, GSE13440, GSE6095. The two additional independent cohorts of 151 transplant biopsies are GSE25902 and GSE1563. Not all samples from all studies were used. Only the samples marked as either AR or STA in each data set were used for analysis.
2013-10-04 | GSE50058 | GEO
Project description:PBMC samples from heart transplant patients were profiled. Sample classification was based on endomyocardial biopsy at the time of sample collection. Keywords = Transplant Keywords = Transplantation Keywords = Heart Transplant Keywords = Graft Rejection Keywords = Rejection Keywords = PBMC Keywords = Immune Response Keywords = Peripheral Blood
2010-06-10 | E-GEOD-2445 | biostudies-arrayexpress
Project description:Long-term survival of the renal allograft is a challenge. A single cell sequencing analysis is a powerful approach to identify genetic/genomic risk for development of long-term graft loss at single cell level. In this study, we compared single cell RNA sequencing profiles of pre-transplant PBMC samples from 4 transplant patients (2 patients with graft loss within 3 years vs 2 patients without graft loss) with simultaneous genome-wide genotype data for common variants to idenitfy the immune cell subtypes and transcriptomic signatures associated with long-term graft loss. These transcriptomic data also integrates with genetic data in an effort to identify genes that mediate the risk for graft survival in a cell-type specific context.
2021-08-29 | GSE182916 | GEO
Project description:PBMC samples from heart transplant patients were profiled. Sample classification was based on endomyocardial biopsy at the time of sample collection. Keywords = Transplant Keywords = Transplantation Keywords = Heart Transplant Keywords = Graft Rejection Keywords = Rejection Keywords = PBMC Keywords = Immune Response Keywords = Peripheral Blood Keywords: other
2005-09-01 | GSE2445 | GEO
Project description:Inducing graft acceptance without chronic immunosuppression remains an elusive goal in organ transplantation. Recent data demonstrate that non-self recognition by graft infiltrating macrophages initiates transplant rejection. Using an experimental transplantation mouse model, we isolated graft-infiltrating macrophages from two transplantation settings: untreated rejecting mice and treated with mTORi-HDL nanobiologics. We used microarrays to detail the global programme of gene expression underlying macrophage dependent organ transplant rejection and identified distinct classes of up-regulated genes during this process, which are down-regulated following tolerogenic treatment with mTORi-HDL nanobiologics.
2018-10-31 | GSE119370 | GEO
Project description:Background: Studies recently support that non-HLA antigens could be additional targets of injury in organ transplant recipients, and MICA was associated with an increased risk of graft loss. Methods: A ProtoArray platform was used to study 37 serum samples from 22 unique patients (15 renal recipients and 7 healthy controls). Thirty paired pre- and post-transplant serum samples were analyzed for detection of de novo post-transplant antibody responses in the 15 patients (10 acute rejection (AR), 5 Stable). Probes on ProtoArray and cDNA platforms (GSE: 3931) were re-annotated and compartment specific gene lists were analyzed using the integrated genomics method. Normal and transplant kidney IHC were performed for MICA antigen localization. Results: Mean MICA-Ab (antibody) signal intensity was significantly higher in transplant patients compared with healthy controls and de novo MICA-Ab were detected in 73% transplant patients. The mean post-transplant signal intensity of MICA-Ab was the highest in C4d+AR. Detection of MICA-Ab responses did not correlate with time post-transplantation, but significantly correlated with decline in graft function over the subsequent year. Integrative genomics predicted localization of the MICA antigen to the glomerulus. IHC confirmed cytoplasmic MICA staining solely in glomerular podocytes in normal kidney. In the transplant kidney, infiltrating mononuclear lymphocytes (T, B and NK) in AR had additional MICA staining. Conclusions: MICA can be highly detected regardless of graft dysfunction or AR. The intensity signal of the MICA antibody correlates with subsequent decline in graft function. The MICA antigen localizes to the glomerulus and infiltrating mononuclear cells in AR.
2009-01-16 | GSE14329 | GEO
Project description:IL-17-producing cells are important mediators of graft-versus-host disease (GVHD) after allogeneic stem cell transplantation (SCT). Here we demonstrate that a distinct CD8+ Tc17 population develops rapidly after SCT but fails to maintain lineage fidelity such that they are unrecognizable in the absence of a fate reporter. Tc17 differentiation is dependent on alloantigen presentation by host-DC together with IL-6. Tc17 cells express high levels of multiple prototypic lineage-defining transcription factors (e.g. RORgt, T-bet) and cytokines (e.g. IL-17A, IL-22, IFNg, GM-CSF, IL-13). Targeted depletion of Tc17 early after transplant protects from lethal acute GVHD, however Tc17 cells are non-cytolytic and fail to mediate graft–versus–leukemia (GVL) effects. Thus, the Tc17 differentiation program during GVHD culminates in a highly plastic, hyper-inflammatory, poorly-cytolytic effector population which we term inflammatory Tc17 (iTc17). Since iTc17 mediate GVHD without contributing to GVL, therapeutic inhibition of iTc17 development in a clinical setting represents an attractive approach for separating GVHD and GVL. Single colour, Illumina MouseRef-8 v2.0 Beadarrays.
2015-09-13 | E-GEOD-70931 | biostudies-arrayexpress