Abstract
Hepatitis C is an infectious disease affecting the liver, caused by the hepatitis C virus (HCV). HCV is an etiological agent of acute and chronic liver disease that exists throughout the world. The high genetic variability of the HCV genome is reflected by six genotypes (1 to 6). Each genotype has a characteristic geographical distribution, which is important epidemiologically. HCV is a blood-borne virus that generally circulates in low titers in the serum of infected individuals. Epidemiologic studies show that the most efficient transmission of HCV is through the transfusion of blood or blood products, the transplantation of organs from infected donors, and the sharing of contaminated needles among injection-drug users. However, fewer than half of patients with acute hepatitis C report a history of such exposure. A small number of epidemiologic studies demonstrate that perinatal, sexual, household, and occupational transmission occurs, but our understanding of the risks of transmission in these settings has been limited. The therapy for chronic hepatitis C has evolved steadily since alpha interferon was first approved for use. At present, the optimal regimen appears to be a 24- or 48-week course of a combined pegylated alpha interferon and ribavirin regimen. Currently, the combination of RNAi (LV-shIRES) with IFN-α has been proposed to prevent therapeutic resistance, and to promote enhanced antiviral activity against HCV. However, any RNAi based therapy may be years away due to off-target effects.
Highlights
The liver and its functionThe liver is the largest glandular organ of the human body and it is the only organ that is able to regenerate to form new tissue
These findings suggest that hepatitis C virus (HCV) takes advantage of the presence of MicroRNA 122 (miR-122) in hepatocytes
Instead of a 5′ cap, the internal ribosome entry site (IRES), located at the 5′ noncoding region of sthe viral genome, plays an essential role in initiating translation [159]. Because it is the most conserved sequence within the viral genome, internal ribosomal entry site (IRES) seems an ideal target for RNA interference (RNAi), and several promising studies have demonstrated inhibition of HCV replication by targeting this region [160]
Summary
The liver is the largest glandular organ of the human body and it is the only organ that is able to regenerate to form new tissue. The E1 and E2 transmembrane domains are composed of two stretches of hydrophobic aa separated by a short polar region containing fully conserved charged residues They have numerous functions, including membrane anchoring, ER localization, and heterodimer assembly [38]. It is suggested that NS5A associates with lipid rafts derived from intracellular membranes through its binding to the Cterminal region of a vesicle membrane-associated protein of 33 kDa (hVAP-33) [76] This interaction appears to be crucial for the formation of the HCV replication complex in connection with lipid rafts [77]. Another report has suggested that the level of NS5A phosphorylation plays an important role in the viral lifecycle by regulating a switch from replication to assembly, whereby hyperphosphorylated forms function to maintain the replication complex in an assemblyincompetent state [79]. NS5B has been found to bind cyclophilin B, a cellular peptidyl-prolyl cis-trans isomerase that apparently regulates HCV replication through modulation of the RNA binding capacity of NS5B [89]
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