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Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype

ABSTRACT: IL28B genotype was shown to be associated with treatment outcome of antiviral thearpy for HCV infection. We tried to clarify the molecular feature that was asocciated with IL2B genotype by comparing Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41804 | GEO | 2013/05/02

SECONDARY ACCESSION(S): PRJNA178219

REPOSITORIES: GEO

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Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype

Project description:IL28B genotype was shown to be associated with treatment outcome of antiviral thearpy for HCV infection. We tried to clarify the molecular feature that was associated with IL2B genotype by comparing Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype. We analyzed ten HCC patients were selected from each IL28B genotype, and their gene expression was determined using Affymetrix genechip analysis.

2013-05-02 | E-GEOD-41804 | biostudies-arrayexpress

Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype

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Primary human hepatocytes treated with IL28B and the HCV JFH1 Genotype 2A clone.

Project description: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 JFHA, and IL28b respectively with three biological replication.

2013-08-16 | E-GEOD-31455 | biostudies-arrayexpress

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Project description:Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype

2015-07-29 | E-GEOD-41804 | ExpressionAtlas

Primary human hepatocytes treated with IL28B and the HCV JFH1 Genotype 2A clone.

2013-08-16 | GSE31455 | GEO

Homo sapiens

Project description:Hepatic gene expression of HCV related Hepatocellular carcinoma and non-cancerous tissue with Il28B rs8099917 TT genotype and TG/GG genotype

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Prolonged activation of innate antiviral gene signature after childbirth is determined by IFNL3 genotype

Project description:Maternal innate and adaptive immune responses are modulated during pregnancy to concurrently defend against infection and tolerate the semi-allogeneic fetus. The restoration of these systems after childbirth is poorly understood. We reasoned that enhanced innate immune activation may extend beyond gestation while adaptive immunity recovers. To test this hypothesis, the transcriptional profiles of total PBMCs following delivery in healthy women were compared to those of non-pregnant control subjects. Interestingly, interferon stimulated genes (ISGs) encoding proteins such as IFIT1, IFIT2, and IFIT3, as well as signaling proteins such as STAT1, STAT2, and MAVS, were enriched postpartum. Antiviral genes were primarily expressed in CD14+ cells and could be stratified according to genetic variation at the interferon-λ3 gene (IFNL3, also named IL28B) single nucleotide polymorphism (SNP) rs12979860. Antiviral gene expression was sustained beyond six months following delivery in mothers with a CT or TT genotype but resembled baseline non-pregnant control levels following delivery in mothers with a CC genotype. CT and TT IFNL3 genotypes have been associated with persistent elevated ISG expression in individuals chronically infected with hepatitis C virus. Together these data suggest that postpartum, the normalization of the physiological rheostat controlling interferon signaling is dependent on IFNL3 genotype.

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Natural killer cell genomic profile is associated with treatment outcome in patients with chronic HCV infection

Project description:Phenotypic and immunogenetic characteristics of NK cells have been recently associated with treatment outcome of HCV infected patients. However, thus far, no global NK patterns predictive of response to antiviral therapy in HCV infection have been identified. We here analyzed phenotypic and transcriptional characteristics of NK cells derived from prospectively followed patients with chronic HCV infection prior to treatment with PEG-IFN/RBV. The results report that the pre-treatment transcriptional patterns of purified NK cells from patients subsequently undergoing a sustained virologic response (SVR) clearly segregated from those of non-responder (NR) patients and surprisingly overlapped with the genomic profile of NK cells from healthy donors and from patients who spontaneously cleared the virus (SR). The treatment outcome was associated with differential surface expression of NKp30 and NKG2D and with the transcriptional expression of molecules involved in post-transcriptional modifications of RNA/protein trafficking and HLA class II signaling. With the development of a highly stringent prediction model (LOOCV p value < 0.00001) we identified a 33 gene signature whose expression predicted with 100% accuracy the outcome of IFN based treatment. None of the genes found to differentiate patients with SVR from NR were related to the IL28B polymorphism. Neither an IL28B CC homozygosis was significantly and clearly associated with SVR in our series of patients. Thus, NK cells are associated to different HCV disease courses and response to treatment and the NK cell evaluation in HCV patients might provide a comprehensive explanation of useful determinants of clinical response in HCV-infected patients subjected to treatment regimens that have IFN as their backbone.

2015-10-01 | GSE51941 | GEO