The transcriptional profiles of chronic HBV patients and asymptomatic carriers
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ABSTRACT:
PROVIDER: PRJNA701914 | ENA |
REPOSITORIES: ENA
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Project description:The study aims at investigating the specifical transcriptional signatures of chronic HBV patients
2021-02-16 | GSE166759 | GEO
Project description:Chronic hepatitis B virus (HBV) infection is a serious global public health problem. To identify susceptibility loci for disease progression of HBV infection, we performed this genome-wide association study using DNA pools of case and control constructed by progressed HBV carriers (acute liver failure, liver cirrhosis, hepatocellular carcinoma) and asymptomatic HBV carriers separately. Performing GWAS on pools of DNA samples is an effective strategy to reduce the costs of studies and pooling DNA has been shown to be an efficient method to select candidate susceptibility loci for follow-up by individual genotyping. Affymetrix Genome-Wide Human Mapping SNP6.0 Arrays were performed for DNA pools, which were constructed by pooling 120 ng DNA from each participant. Four independent pools were created: case A was acute liver failure group (n = 86), case B was liver cirrhosis group (n = 88), case C was hepatocellular carcinoma group (n = 90) and case D was asymptomatic HBV carriers (n = 66) that was considered as control. Twelve chips (each pool was replicated in triplicate) were finished according to the manufacturer's instruction.
2013-12-10 | E-GEOD-26034 | biostudies-arrayexpress
Project description:genomic profiles of Staphylococcus aureus isolates from asymptomatic carriers in Switzerland
2020-04-08 | E-MTAB-8960 | biostudies-arrayexpress
Project description:Chronic hepatitis B virus (HBV) infection is a serious global public health problem. To identify susceptibility loci for disease progression of HBV infection, we performed this genome-wide association study using DNA pools of case and control constructed by progressed HBV carriers (acute liver failure, liver cirrhosis, hepatocellular carcinoma) and asymptomatic HBV carriers separately. Performing GWAS on pools of DNA samples is an effective strategy to reduce the costs of studies and pooling DNA has been shown to be an efficient method to select candidate susceptibility loci for follow-up by individual genotyping.
2013-12-10 | GSE26034 | GEO
Project description:We compared transcriptome of monocyte-derived macrophages of 5 patients with GBA-PD (4 L444P/N, 1 N370S/N) and 4 asymptomatic GBA mutation carriers (GBA-carriers) (3 L444P/N, 1 N370S/N) and 4 controls. We also conducted comparative transcriptome analysis for L444P/N only GBA-PD patients and GBA-carriers. Revealed deregulated genes in GBA-PD independently of GBA mutations (L444P or N370S) were involved in immune response, neuronal function. We found upregulated pathway associated with zinc metabolism in L444P/N GBA-PD patients. The potential important role of DUSP1 in the pathogenesis of GBA-PD was suggested.
2021-09-29 | GSE184956 | GEO
Project description:We compared transcriptome of monocyte-derived macrophages of 5 patients with GBA-PD (4 L444P/N, 1 N370S/N) and 4 asymptomatic GBA mutation carriers (GBA-carriers) (3 L444P/N, 1 N370S/N) and 4 controls. We also conducted comparative transcriptome analysis for L444P/N only GBA-PD patients and GBA-carriers. Revealed deregulated genes in GBA-PD independently of GBA mutations (L444P or N370S) were involved in immune response, neuronal function. We found upregulated pathway associated with zinc metabolism in L444P/N GBA-PD patients. The potential important role of DUSP1 in the pathogenesis of GBA-PD was suggested.
2021-10-12 | E-MTAB-11029 | biostudies-arrayexpress
Project description:The low frequency of HBV-specific CD8+ T cells in the peripheral blood of CHB patients has limited studies of the mechanisms underlying HBV-induced T cell exhaustion. Similar to the expansion defect displayed in HBV-specific CD8+ T cells, TCR-induced proliferation of global CD8+ T cells is impaired in a fraction of chronic HBV (CHB) patients. Thus, examining the molecular regulation of global CD8+ T cell function in CHB patients may provide insight into the exhaustion of HBV-specific CD8+ T cells. We used microarrays to detail the global programme of gene expression of CD8 T cells from CHB patients who have not received anti-viral treatment. Fifteen milliliters of blood was drawn from eachof three CHB patients and three healthy donors. PBMCs were enriched using Ficoll, and CD8+ T cells were purified using positive selection beads to a purity of >95% (Miltenyi Biotec, Auburn, CA). Total RNA was extracted using a mirVana isolation kit (Life Technologies, Carlsbad, CA).
2016-07-01 | E-GEOD-51489 | biostudies-arrayexpress
Project description:The low frequency of HBV-specific CD8+ T cells in the peripheral blood of CHB patients has limited studies of the mechanisms underlying HBV-induced T cell exhaustion. Similar to the expansion defect displayed in HBV-specific CD8+ T cells, TCR-induced proliferation of global CD8+ T cells is impaired in a fraction of chronic HBV (CHB) patients. Thus, examining the molecular regulation of global CD8+ T cell function in CHB patients may provide insight into the exhaustion of HBV-specific CD8+ T cells. We used microarrays to detail the global programme of gene expression of CD8 T cells from CHB patients who have not received anti-viral treatment.
2016-07-01 | GSE51489 | GEO
Project description:Importance: An intronic hexanucleotide repeat expansion (HRE) in C9orf72 is the commonest monogenic cause of the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Predicting those who will develop neurodegeneration and its timing will be essential to initiating and assessing preventative therapy. This requires consideration of both compensatory, protective mechanisms and pathogenic events prior to overt neurodegeneration. Objective: To identify biochemical changes in individuals at higher risk of developing ALS or FTD via C9orf72 HRE heterozygosity. Design: Cross sectional observational study. Setting: Tertiary ALS or dementia referral centre. Participants: People with established ALS or FTD, either due to C9orf72 HRE or apparently sporadic cases; asymptomatic first-degree relatives of those with a known C9orf72 HRE; asymptomatic non-carrier controls. Exposure: C9orf72 HRE. Main outcomes: Relative abundance of 30 predefined cerebrospinal fluid biomarkers of ALS and FTD comparing asymptomatic C9orf72 HRE carriers and age-matched non-carriers. Differential abundance of proteins quantified using data independent acquisition mass spectrometry and neurofilament light chain measured by electrochemiluminescent assay. Results: Data for 19 people with sporadic ALS, 10 people with C9orf72 ALS, 14 people with sporadic FTD, 10 people with C9orf72 FTD, 48 asymptomatic C9orf72 HRE carriers and 39 non-carrier controls were analysed. Ubiquitin carboxyl-hydrolase isozyme L1 levels were higher in asymptomatic C9orf72 HRE carriers compared with age-matched non-carriers (log2fold change 0.20, FDR-adjusted p-value = 0.034). Neurofilament light chain levels did not differ significantly between groups. Ubiquitin carboxyl-hydrolase isozyme L1 levels remained elevated after exclusion of those with high neurofilament light chain levels, after adjusting for NFL level and after adjusting for age. Conclusions and relevance: Elevated cerebrospinal fluid ubiquitin carboxyl-hydrolase isozyme L1 levels in C9orf72 hexanucleotide repeat expansion carriers occurs in the absence of elevation in neurofilament light chain, potentially reflecting mechanisms that precede the phase of neurodegeneration characterised by rapid neuronal loss. Such mechanisms may have either compensatory or pathogenic roles. Ubiquitin carboxyl-terminal hydrolase isozyme L1 elevation brings forward the window on the changes associated with the C9orf72 HRE carrier state, with the potential to inform understanding penetrance and approaches to prevention.
2024-11-19 | PXD051859 | Pride
Project description:HBV-specific CD8 cells are deeply exhausted in chronic hepatitis B and their function can only be partially corrected by modulation of up-regulated inhibitory pathways, suggesting a more complex molecular interplay. With the aim of identifying more suitable molecular targets to correct T cell dysfunction, we compared the transcriptome profile of HBV-specific CD8 cells of acute and chronic patients with the reference profile of HBV- and Flu-specific CD8 cells from patients able to resolve HBV infection spontaneously and from healthy subjects. The results indicate that exhausted HBV-specific CD8 cells are deeply impaired at a metabolic and energetic level with a prevalent down-regulation of different key cellular processes centered on an extensive alteration of mitocondrial functions. Mitochondrial modulation by antioxidant compounds could improve significantly the HBV-specific T cell function with minimal effect on T cells of different specificity. The results identify mitochondria as ideal targets for functional T cell reconstitution strategies to cure HBV infection
2017-01-11 | GSE67801 | GEO