Gene expression profile of Huh‐7 cells expressing hepatitis C virus genotype 1b or 3a core proteins

Abstract

The expression of HCV core proteins of different genotypes leads to a specific gene expression profile. This may account for the variable disease expression associated with HCV infection.

Hepatitis C virus core protein genotype 3a increases SOCS-7 expression through PPAR- in Huh-7 cells

“…We have chosen 48 h as the time point for study because the maximum expression level of HCV core protein after transfection was reached (Fig. 1a), consistent with our previous findings (Abid et al, 2005;Pazienza et al, 2007Pazienza et al, , 2009). …”

“…It has been shown that growing cells in delipidated medium reduce the triglyceride accumulation induced by HCV core protein genotype 3a, suggesting a lack of de novo synthesis of triglycerides (Abid et al, 2005) and suggesting that the core protein seems to promote a mere redistribution of fat-laden vesicles typically found in Huh-7 cells, rather than a true triglyceride accumulation. On the other hand, the core protein alone is able to modulate the expression of several cellular genes involved in lipid metabolism (Pazienza et al, 2009) and/or to promote de novo triglyceride synthesis (Lerat et al, 2009). …”

“…In the present study, we intended to investigate whether the last member of the SOCS family, SOCS-7, which we recently demonstrated to be upregulated in human hepatoma Huh-7 cells expressing the HCV core protein of genotype 3a (Pazienza et al, 2009) and which is involved in the degradation of insulin receptor substrate 1 (IRS-1) (Pazienza et al, 2007) [one of the major players in the regulation of hepatic metabolism by insulin (Taniguchi et al, 2005)], is activated by the same JAK/STAT pathway. Moreover, as we and others have recently uncovered a role in HCV infection for peroxisome proliferator-activated receptor gamma (PPAR-c) (de Gottardi et al, 2006;Pazienza et al, 2007;Dharancy et al, 2009), a member of the nuclear PPAR family and a promising therapeutic target for the inhibition of liver glucose production during metabolic syndrome (Edgerton et al, 2009), we tested the role of this nuclear receptor in HCV-induced SOCS-7 upregulation.…”

Genome-Wide Analysis of Host mRNA Translation during Hepatitis C Virus Infection

“…HCV replication and viral protein expression lead to differential expression of host genes as determined by microarray or proteomic studies (1)(2)(3). A breakthrough in HCV research was the discovery of an HCV strain, JFH1, capable of replicating efficiently and of producing viral particles in cultured cells (4)(5)(6).…”

Steatosis and insulin resistance in hepatitis C: A way out for the virus?

“…Using microarray analysis Pazienza et al [15] compared the gene expression profile of Huh7 cells transfected with the core protein of HCV genotype 1b and 3a, leading to the conclusion that several genes involving lipid transport and metabolism were up-or down-regulated in a genotypespecific manner. This fact could explain the variable disease expression associated with HCV infection.…”