scholarly journals Gene Expression Profiling of Endoplasmic Reticulum Stress in Hepatitis C Virus-Containing Cells Treated with an Inhibitor of Protein Disulfide Isomerases

ACS Omega ◽  
2018 ◽  
Vol 3 (12) ◽  
pp. 17227-17235 ◽  
Author(s):  
Dennis Özcelik ◽  
Andrew Seto ◽  
Bojana Rakic ◽  
Ali Farzam ◽  
Frantisek Supek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endoplasmic Reticulum ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Endoplasmic Reticulum Stress ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Protein Disulfide Isomerases ◽  
Disulfide Isomerases ◽  
Protein Disulfide

scholarly journals Gene Expression Profiling of Different Huh7 Variants Reveals Novel Hepatitis C Virus Host Factors

Viruses ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 36
Author(s):  
Christopher Dächert ◽  
Evgeny Gladilin ◽  
Marco Binder
Keyword(s):  
Gene Expression ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Gene Expression Profiling ◽  
Cell Line ◽  
Expression Profiling ◽  
Hepatoma Cell ◽  
Host Factors ◽  
Hepatoma Cell Line ◽  
Huh7 Cells

Chronic Hepatitis C virus (HCV) infection still constitutes a major global health problem with almost half a million deaths per year. To date, the human hepatoma cell line Huh7 and its derivatives is the only cell line that robustly replicates HCV. However, even different subclones and passages of this single cell line exhibit tremendous differences in HCV replication efficiency. By comparative gene expression profiling using a multi-pronged correlation analysis across eight different Huh7 variants, we identified 34 candidate host factors possibly affecting HCV permissiveness. For seven of the candidates, we could show by knock-down studies their implication in HCV replication. Notably, for at least four of them, we furthermore found that overexpression boosted HCV replication in lowly permissive Huh7 cells, most prominently for the histone-binding transcriptional repressor THAP7 and the nuclear receptor NR0B2. For NR0B2, our results suggest a finely balanced expression optimum reached in highly permissive Huh7 cells, with even higher levels leading to a nearly complete breakdown of HCV replication, likely due to a dysregulation of bile acid and cholesterol metabolism. Our unbiased expression-profiling approach, hence, led to the identification of four host cellular genes that contribute to HCV permissiveness in Huh7 cells. These findings add to an improved understanding of the molecular underpinnings of the strict host cell tropism of HCV.

Gene Expression Profiling of Immune Responsive and Fibrosis Genes in Hepatitis C Virus Infected Patients

2014 ◽  
Vol 27 (5) ◽  
pp. 250-254 ◽  
Author(s):  
Sobia Idrees ◽  
Usman Ali Ashfaq ◽  
Muhammad Shareef Masoud ◽  
Muhammad Qasim ◽  
Tariq Javed ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Gene Expression Profiling ◽  
Expression Profiling

scholarly journals Increasing Melanoma Cell Death Using Inhibitors of Protein Disulfide Isomerases to Abrogate Survival Responses to Endoplasmic Reticulum Stress

2008 ◽  
Vol 68 (13) ◽  
pp. 5363-5369 ◽  
Author(s):  
Penny E. Lovat ◽  
Marco Corazzari ◽  
Jane L. Armstrong ◽  
Shaun Martin ◽  
Vittoria Pagliarini ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Endoplasmic Reticulum Stress ◽  
Melanoma Cell ◽  
Protein Disulfide Isomerases ◽  
Disulfide Isomerases ◽  
Protein Disulfide

scholarly journals Gene Expression Profiling Indicates the Roles of Host Oxidative Stress, Apoptosis, Lipid Metabolism, and Intracellular Transport Genes in the Replication of Hepatitis C Virus

2010 ◽  
Vol 84 (10) ◽  
pp. 5404-5414 ◽  
Author(s):  
Samantha Blackham ◽  
Andrew Baillie ◽  
Fadel Al-Hababi ◽  
Katja Remlinger ◽  
Shihyun You ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatitis C Virus ◽  
Lipid Metabolism ◽  
Hepatitis C ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Intracellular Transport ◽  
Hcv Infection ◽  
Replication Cycle ◽  
Host Genes

ABSTRACT Hepatitis C virus (HCV) is a leading cause of chronic liver disease. The identification and characterization of key host cellular factors that play a role in the HCV replication cycle are important for the understanding of disease pathogenesis and the identification of novel antiviral therapeutic targets. Gene expression profiling of JFH-1-infected Huh7 cells by microarray analysis was performed to identify host cellular genes that are transcriptionally regulated by infection. The expression of host genes involved in cellular defense mechanisms (apoptosis, proliferation, and antioxidant responses), cellular metabolism (lipid and protein metabolism), and intracellular transport (vesicle trafficking and cytoskeleton regulation) was significantly altered by HCV infection. The gene expression patterns identified provide insight into the potential mechanisms that contribute to HCV-associated pathogenesis. These include an increase in proinflammatory and proapoptotic signaling and a decrease in the antioxidant response pathways of the infected cell. To investigate whether any of the host genes regulated by infection were required by HCV during replication, small interfering RNA (siRNA) silencing of host gene expression in HCV-infected cells was performed. Decreasing the expression of host genes involved in lipid metabolism (TXNIP and CYP1A1 genes) and intracellular transport (RAB33b and ABLIM3 genes) reduced the replication and secretion of HCV, indicating that they may be important factors for the virus replication cycle. These results show that major changes in the expression of many different genes in target cells may be crucial in determining the outcome of HCV infection.

Sign in / Sign up

Export Citation Format

Share Document