<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/017/SRR12247917/SRR12247917_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/018/SRR12247918/SRR12247918_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/019/SRR12247919/SRR12247919_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/016/SRR12247916/SRR12247916_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/021/SRR12247921/SRR12247921_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/020/SRR12247920/SRR12247920_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/017/SRR12247917/SRR12247917_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/016/SRR12247916/SRR12247916_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/018/SRR12247918/SRR12247918_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/021/SRR12247921/SRR12247921_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/020/SRR12247920/SRR12247920_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR122/019/SRR12247919/SRR12247919_1.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>Hepatology, The Third Hospital of Hebei Medical University</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA646928</full_dataset_link><scientific_name>Homo sapiens</scientific_name><tag>xref:PubMed:33015132</tag><long_description>Hepatitis C virus (HCV) infection is an important etiology of chronic liver disease. Multiple possible molecular mechanisms were involved in the progression of liver fibrosis in chronically HCV-infected patients. Therefore, the further revealing novel genes for regulating liver fibrosis might provide evidence for gene diagnosis and molecular-targeted therapy. In this study, we examined the differentially expressed mRNA in plasma samples from the healthy control and patients with HCV-related liver fibrosis, in order to explore the potential predicted and therapeutic target for the development of HCV-related liver fibrosis. Overall design: Plasma samples from HCV patients with moderate to severe liver fibrosis (F3-4) and healthy control subjects (each group included 3 cases) were used for whole transcript digital gene expression (DGE) profiling sequencing.</long_description><repository>ENA</repository><description_synonyms>human hepatitis C virus HCV, human hepatitis C virus, hepatitis C virus HCV, Gene Expressions, Patient, determination, Liver fibrosis., Clients, chemical analysis, post-transfusion hepatitis non A non B virus, Gene, Expression, assay, HCV, Expressions, Client, Hepatitis C</description_synonyms><name_synonyms>human hepatitis C virus HCV, human hepatitis C virus, hepatitis C virus HCV, Gene Expressions, Patient, determination, Liver fibrosis., Clients, chemical analysis, post-transfusion hepatitis non A non B virus, Gene, Expression, assay, HCV, Expressions, Client, Hepatitis C</name_synonyms></additional><is_claimable>false</is_claimable><name>Digital Gene Expression profiles analysis of patients with HCV-related hepatic fibrosis</name><description>Digital Gene Expression profiles analysis of patients with HCV-related hepatic fibrosis</description><dates><last_updated>2025-09-24</last_updated><first_public>2020-09-12</first_public></dates><accession>PRJNA646928</accession><cross_references><GEO>GSE154055</GEO><taxon>9606</taxon><PubMed>33015132</PubMed></cross_references></HashMap>