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Cellular gene expression during Hepatitis C Virus replication revealed by Ribosome profiling

ABSTRACT: Cellular gene expression during Hepatitis C Virus replication revealed by Ribosome profiling

PROVIDER: PRJNA525090 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8649960.fastq.gz	Fastqsanger.gz
	SRR8649961.fastq.gz	Fastqsanger.gz
	SRR8649962.fastq.gz	Fastqsanger.gz
	SRR8649963.fastq.gz	Fastqsanger.gz
	SRR8649954.fastq.gz	Fastqsanger.gz

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Cellular gene expression during Hepatitis C Virus replication revealed by Ribosome profiling

Project description:Background: Hepatitis C virus (HCV) infects human liver hepatocytes, often leading to liver cirrhosis and hepatocellular carcinoma (HCC). It is believed that chronic infection alters host gene expression and favours HCC development. In particular, HCV replication in Endoplasmic Reticulum (ER) derived membranes induces chronic ER stress. How HCV replication affects host mRNA translation and transcription at a genome wide level is not yet known. Methods: We used Riboseq (Ribosome Profiling) to analyze transcriptome and translatome changes in Huh-7.5 hepatoma cells replicating HCV for 6 days. Results: Established viral replication does not cause global changes in host gene expression - only around 30 genes are differentially expressed. Upregulated genes are related to ER stress, HCV replication and HCC development. Some mRNAs (PPP1R15A/GADD34, DDIT3/CHOP, TRIB3) may be subject to uORF mediated translation control in response to stress-induced eIF2 inactivation. Transcriptional downregulation mainly affects mitochondrial respiratory chain complex genes. Conclusion: After establishing HCV replication, cellular gene expression is reprogrammed towards stress response and HCC development. Downregulation of mitochondrial respiratory chain genes indicates how a virus induces cancer cell-like metabolic reprogramming ("Warburg effect"). Thus, HCV escapes stress response pathways but induces selective gene expression changes which likely are beneficial for chronic infection and cancerogenesis.

2019-03-02 | GSE127713 | GEO

Cellular Gene Expression during Hepatitis C Virus Replication as Revealed by Ribosome Profiling.

Project description:BACKGROUND:Hepatitis C virus (HCV) infects human liver hepatocytes, often leading to liver cirrhosis and hepatocellular carcinoma (HCC). It is believed that chronic infection alters host gene expression and favors HCC development. In particular, HCV replication in Endoplasmic Reticulum (ER) derived membranes induces chronic ER stress. How HCV replication affects host mRNA translation and transcription at a genome wide level is not yet known. METHODS:We used Riboseq (Ribosome Profiling) to analyze transcriptome and translatome changes in the Huh-7.5 hepatocarcinoma cell line replicating HCV for 6 days. RESULTS:Established viral replication does not cause global changes in host gene expression-only around 30 genes are significantly differentially expressed. Upregulated genes are related to ER stress and HCV replication, and several regulated genes are known to be involved in HCC development. Some mRNAs (PPP1R15A/GADD34, DDIT3/CHOP, and TRIB3) may be subject to upstream open reading frame (uORF) mediated translation control. Transcriptional downregulation mainly affects mitochondrial respiratory chain complex core subunit genes. CONCLUSION:After establishing HCV replication, the lack of global changes in cellular gene expression indicates an adaptation to chronic infection, while the downregulation of mitochondrial respiratory chain genes indicates how a virus may further contribute to cancer cell-like metabolic reprogramming ("Warburg effect") even in the hepatocellular carcinoma cells used here.

| S-EPMC6470931 | biostudies-literature

Hepatitis Delta Virus histone mimicry drives the recruitment of chromatin remodelers for viral RNA replication

Project description:Hepatitis Delta virus (HDV) is a satellite of Hepatitis B virus with a single stranded circular RNA genome. HDV RNA genome synthesis is carried out in infected cells by cellular RNA polymerases with the assistance of the small hepatitis delta antigen (S-HDAg). Here we show that S-HDAg binds the Bromodomain (BRD) Adjacent To Zinc Finger Domain 2B (BAZ2B) protein, a regulatory subunit of BRF (BAZ2B-Associated Remodeling Factor) ISWI chromatin remodeling complexes. ShRNAs-mediated silencing of BAZ2B or its inactivation with the BAZ2B-BRD inhibitor GSK-2801 impairs HDV replication in HDV-infected human hepatocytes. S-HDAg contains a short linear interacting motif (SLiM) KacXXR, similar to the one recognized by BAZ2B-BRD in histone H3. We found that the integrity of the S-HDAg SLiM sequence is required for S-HDAg interaction with BAZ2B-BRD and for HDV RNA replication. Our results suggest that S-HDAg uses a histone mimicry strategy to co-activate the RNA Polymerase II-dependent synthesis of HDV RNA and sustain HDV replication.

2020-05-27 | PXD016880 | Pride

Circadian control of hepatitis B virus replication

Project description:Circadian control of hepatitis B virus replication

| PRJNA685550 | ENA

Regulation of Translation Elongation Revealed by Ribosome Profiling

Project description:Regulation of Translation Elongation Revealed by Ribosome Profiling

| PRJNA473984 | ENA

MicroRNA-27a regulates lipid metabolism and inhibits hepatitis C virus replication in human hepatoma cells

Project description:Gene expression profiling was carried out in Huh-7.5 cells in which miR-27a was over- or under-expressed. Transfection of cells with pre-miR-27a and pre-miR-control, or anti-miR-27a and anti-miR-control enabled down- and up-regulated genes to be determined, respectively. Replication and infectivity of the lipotrophic hepatitis C virus (HCV) is regulated by cellular lipid status. Among differentially expressed micro (mi)RNAs, we found that miR-27a was preferentially expressed in HCV-infected compared with hepatitis B virus (HBV)-infected liver. Gene expression profiling of Huh-7.5 cells showed that miR-27a regulates lipid metabolism by targeting the lipid synthetic transcriptional factor, RXRα, and the lipid transporter, ABCA1

2013-06-05 | GSE41737 | GEO

Regulation of Translation Elongation Revealed by Ribosome Profiling [Dataset_1]

Project description:Regulation of Translation Elongation Revealed by Ribosome Profiling [Dataset_1]

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Regulation of Translation Elongation Revealed by Ribosome Profiling [Dataset_3]

Project description:Regulation of Translation Elongation Revealed by Ribosome Profiling [Dataset_3]

| PRJNA473987 | ENA

Regulation of Translation Elongation Revealed by Ribosome Profiling [Dataset_2]

Project description:Regulation of Translation Elongation Revealed by Ribosome Profiling [Dataset_2]

| PRJNA473988 | ENA

Regulation of Translation Elongation Revealed by Ribosome Profiling [Dataset_4]

Project description:Regulation of Translation Elongation Revealed by Ribosome Profiling [Dataset_4]