{"owner": "ArrayExpress Uploader", "ownerprofile_id": "arrayexpress_sid", "species": "human", "factors": [{"GSM773317": {"time": "  ", "compound": "none"}}, {"GSM773317": {"time": "  ", "compound": "none"}}, {"GSM773317": {"time": "  ", "compound": "none"}}, {"GSM773320": {"time": "24", "compound": "IFN"}}, {"GSM773320": {"time": "24", "compound": "IFN"}}, {"GSM773320": {"time": "24", "compound": "IFN"}}, {"GSM773323": {"time": "6", "compound": "IFN"}}, {"GSM773323": {"time": "6", "compound": "IFN"}}, {"GSM773323": {"time": "6", "compound": "IFN"}}, {"GSM773326": {"time": "24", "compound": "IL28B"}}, {"GSM773326": {"time": "24", "compound": "IL28B"}}, {"GSM773326": {"time": "24", "compound": "IL28B"}}, {"GSM773329": {"time": "6", "compound": "IL28B"}}, {"GSM773329": {"time": "6", "compound": "IL28B"}}, {"GSM773329": {"time": "6", "compound": "IL28B"}}], "id": 4192, "pop_total": 0, "platform": 4, "summary_wrapped": "Recent identification of IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III...", "pubmed_id": 22248663, "geo_gse_id": "E-GEOD-31193", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 2, "sample_count": 15, "tags": ["hepatitis", "hepatitis c", "liver"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_id_plat": "E-GEOD-31193_A-AFFY-44", "slug": "transcription-profiling-by-array-of-primary-human", "geo_gds_id": "", "name": "Transcription profiling by array of primary human hepatocytes derived from hepatitis C patients treated with type III interferons (IFNs) for 6 or 24 hours", "created": "Sep.16, 2014", "summary": "Recent identification of IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III interferons (IFNs) in hepatitis C infection. The function of type III IFNs in intrinsic antiviral immunity is poorly understood.  Here we show that HCV infection of primary human hepatocytes results in a robust induction of type III but not type I IFNs, leading to IFN- stimulated gene (ISG) expression.  In addition, HCV infection elicits a much broader range of gene expression alterations in addition to ISG induction. The induction of type III IFNs is mediated by IRF3 and NFkB- dependent pathways.  Type III IFN, aside from upregulating ISGs with a different kinetic profile, induces a distinct set of genes from type I IFN, potentially explaining the functional difference between the two types of IFNs. Chimpanzees undergoing experimental HCV infection demonstrated a prompt hepatic induction of IL28, associating with ISG upregulation, but minimal type I IFN induction. Analysis of liver biopsies from HCV-infected patients supported a close correlation among hepatic expression of IL28 and ISGs, but not with type I IFNs.    Our study demonstrates that HCV infection results predominantly in type III IFN induction in the liver and the level of induction correlates with hepatic ISG levels, thus providing a mechanistic explanation for the association between IL28, ISG levels and recovery from HCV infection as well as a potential therapeutic strategy for the treatment of non-responders. Samples were treated with IFN or IL28b after 6 or 24 hours with three replications", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-31193", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-31193/samples/"}