No HCV-1 Subtype Misclassification by LiPA 2.0
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ABSTRACT:
PROVIDER: PRJEB21943 | ENA |
REPOSITORIES: ENA
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Project description:Introduction: Mechanisms that contribute to the pathogenesis of liver damage caused by hepatitis C virus (HCV) are not fully understood. Our previous work on liver biopsies from chronic HCV patients has shown modulation of the expression of certain cell cycle proteins indicating HCV-induced modifications of cell cycle events. We therefore hypothesize that HCV infection disrupts normal regulation of cell cycle that contributes to disease progression. Objective: To identify molecular disruptions during the course of HCV-associated disease progression, using liver biopsy specimens of chronic hepatitis C patients. Methods: Liver biopsy samples classified on histological basis as early (fibrosis stage 0-1) or advanced (fibrosis stage 3-4) disease stage were studied using oligonucleotide array ( HG U133 Plus 2.0, Affymetrix GeneChip™ System). For comparison, liver specimens from patients with non-viral hepatitis were also analyzed by microarray. Expression data was analyzed using Genespring (GX 7.2) and Ingenuity Pathway analysis (3.0). The differential expression of selected cell cycle genes (cyclin D2, KPNA2, HERC5 and Bcl-2) identified after microarray analysis was confirmed by quantitative real-time RT-PCR. Results: Microarray analysis revealed two-fold or greater transcriptional change in 792 genes of the total 38,500 known human genes in HCV-advance disease stage (HCV-A) as compared to HCV-early disease stage (HCV-E). Most of the genes have a defined role in immune response, extracellular matrix and cell cycle and apoptosis. Keywords: HCV-advance disease state
2007-11-01 | GSE7741 | GEO
Project description:The purpose of the study is to examine the efficacy of educational materials to promote hepatitis C virus (HCV) screening and colorectal cancer (CRC) screening uptake among adults born between 1945-1965.
| 2384707 | ecrin-mdr-crc
Project description:Introduction: Mechanisms that contribute to the pathogenesis of liver damage caused by hepatitis C virus (HCV) are not fully understood. Our previous work on liver biopsies from chronic HCV patients has shown modulation of the expression of certain cell cycle proteins indicating HCV-induced modifications of cell cycle events. We therefore hypothesize that HCV infection disrupts normal regulation of cell cycle that contributes to disease progression. Objective: To identify molecular disruptions during the course of HCV-associated disease progression, using liver biopsy specimens of chronic hepatitis C patients. Methods: Liver biopsy samples classified on histological basis as early (fibrosis stage 0-1) or advanced (fibrosis stage 3-4) disease stage were studied using oligonucleotide array ( HG U133 Plus 2.0, Affymetrix GeneChip⢠System). For comparison, liver specimens from patients with non-viral hepatitis were also analyzed by microarray. Expression data was analyzed using Genespring (GX 7.2) and Ingenuity Pathway analysis (3.0). The differential expression of selected cell cycle genes (cyclin D2, KPNA2, HERC5 and Bcl-2) identified after microarray analysis was confirmed by quantitative real-time RT-PCR. Results: Microarray analysis revealed two-fold or greater transcriptional change in 792 genes of the total 38,500 known human genes in HCV-advance disease stage (HCV-A) as compared to HCV-early disease stage (HCV-E). Most of the genes have a defined role in immune response, extracellular matrix and cell cycle and apoptosis. Experiment Overall Design: Liver biopsy samples were collected from patients of (a) HCV-infected early disease stage (HCV-E, control 1) (b) non-HCV advance disease stage (control 2) and (c) HCV-infected advance disease stage (HCV-A) for RNA extraction. Equal amount of RNA was pooled from samples (n=4)within each group and hybridized to HG-U133 Plus 2.0 array.
2008-06-15 | E-GEOD-7741 | biostudies-arrayexpress
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2012-05-02 | E-GEOD-37715 | biostudies-arrayexpress
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2017-06-21 | PXD005777 | Pride
Project description:HCV+ cells were detected by smiFISH on liver section of a patient with hepatocellular carcinoma. Clusters of HCV+ and HCV- cells were captured by laser microdissection and transriptomes analysed by RNA sequening. Highly sensitive single molecule fluorescent in situ hybridization applied to frozen tissue sections of a hepatitis C patient allowed the delineation of clusters of infected hepatocytes. Laser micro-dissection followed by RNAseq analysis of HCV-positive and -negative regions from the tumoral and non-tumoral tissues from the same patient revealed HCV-related deregulation of expression of genes in the tumor and in the non-tumoral tissue.
2022-01-31 | GSE192862 | GEO
Project description:Primary human hepatocytes (PHHs) are a liver-specific cell subtype, and we have shown that these cells respond in a unique manner to the introduction of hepatitis C viral RNA (HCV vRNA) derived from different genotypes of the virus. We used microarray to analyze the transcriptional differences between the PHHs exposed to the different genotypes of HCV to further shed light on their differential effects on HCV innate immune responses in vitro HCV vRNA from either genotype 3a HCV or genotype 1a HCV was introduced into the PHH cells for 8 hours. Total RNA was then harvested to determine transcriptional differences.
2014-12-20 | E-GEOD-64400 | biostudies-arrayexpress
Project description:The role of chronic hepatitis C virus (HCV) in the pathogenesis of HCV-associated hepatocellular carcinoma (HCC) is not completely understood, particularly at the molecular level. We studied gene expression in normal, pre-malignant (cirrhosis), and tumor (HCC) liver tissues using Affymetrix GeneChips. Keywords: cross-sectional
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Project description:Using RNA-Seq, we examined the transcriptome profiles of human iPSC-derived macrophage (IPSDM) with knockout of the LIPA gene by CRISPR/Cas9 gene editing technologies.
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Project description:Cytosolic lipid droplets (LDs) are vital to Hepatitis C Virus (HCV) infection as the putative sites of virion assembly. To identify novel regulators of HCV particle production, we performed quantitative LD proteome analysis. Huh7.5 cells were labeled by stable isotope labeling with heavy amino acids in cell culture (SILAC) and subsequently infected with an HCV Jc1 reporter virus. After selection for HCV-infected cells, equal amounts of HCV-infected and uninfected control cells were mixed, LDs were isolated and analyzed by LC-ESI-MS/MS.
2016-09-26 | PXD004707 | Pride