Abstract
The hepatitis C virus (HCV) is known as a main etiological cause of chronic hepatitis. HCV infection disturbs cholesterol metabolism of the host, which is frequently observed in patients suffering from chronic hepatitis C (CHC). The course of viral infections remains under strict control of microRNA (miRNA). In the case of HCV, miR-122 exerts a positive effect on HCV replication in vitro. The purpose of this study was to investigate the impact of peginterferon alpha (pegIFN-α) and ribavirin treatments on the expression of miR-122 and the cholesterol level in the peripheral blood mononuclear cells (PBMCs) of CHC patients. We report here that the level of miR-122 expression in the PBMCs decreased after the antiviral treatment in comparison to the pretreated state. Simultaneously, the level of cholesterol in the PBMCs of CHC patients was higher six months following the treatment than it was pretreatment. Consequently, it seems that the decrease of miR-122 expression in the PBMCs of CHC patients is one of the antiviral effects connected with the pegIFN-alpha/ribavirin treatments.
Highlights
180 million people worldwide are known to be infected with the hepatitis C virus (HCV), which is a main etiological cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma [1]
HCV RNA replication and virion assembly depend on the products of the cholesterol pathway, such as cholesterol and geranylgeranyl pyrophosphate [6]; HCV assembly requires a platform of cellular lipid droplets that result in a considerable alteration of host lipid metabolism [7]
Our findings indicated that the the intracellular cholesterol level in the peripheral blood mononuclear cells (PBMCs) of chronic hepatitis C (CHC) patients was significantly higher, and miR-122 intracellular cholesterol level in the PBMCs
Summary
180 million people worldwide are known to be infected with the hepatitis C virus (HCV), which is a main etiological cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma [1]. The development of chronic hepatitis C (CHC) infection is strictly associated with an ineffective immunological response, as well as with lipid disorders of hosts [2]. The HCV particles bind to lipoproteins to form lipoviroparticles (LVPs) [3] and use various host surface receptors, such as the low-density lipoprotein receptor [4] and the scavenger B receptor [5], as important entry factors. In addition to cirrhosis and hepatocellular carcinoma, HCV infection is frequently characterized by disorders such as hepatic steatosis and hypocholesterolemia [2].
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