Analysis of the Intracellular Zinc in HCV Replicon
Hepatitis C virus (HCV) is one of the most prevalent cause of liver diseases with estimates
placing nearly 3% of the world population, roughly 150 million people, as HCV-infected.
Persistent HCV infection eventually develops into liver cirrhosis or hepatocellular carcinoma
and more than 700,000 people die every year from hepatitis C-related liver diseases.
On the other hand patients with chronic liver disease tend to be complicated with metabolic
disturbance of trace element, namely the decrease of zinc and the increase of iron and copper.
We have reported zinc supplementation additively enhanced the effect of interferon (IFN) on
the eradication of HCV.
Zinc is the component not only of non-structural protein NS3 of HCV but also of an inducer of metallothionein, which is an antioxidant and a chelating agent of metals.
As for iron, phlebotomy could improve the liver function due to iron depletion through
the reduction of oxidative stress.
Copper increases and deposits the hepatocytes as liver disease progresses
not only in Wilson’s disease but chronic viral hepatitis.
In vitro assay of HCV has long been difficult to establish because no cell culture system
could replicate HCV until Bartenschlager developed in vitro
HCV-replication system called “replicon” which cannot produce
the complete virion of HCV but efficiently expressed a part of
structural and nonstructural proteins of HCV in Huh-7 hepatoma cell line.
This system is useful for pharmacological assessment of drug effect on HCV but in order to reproduce the cellular event by HCV replicon, we used the full genome HCV replicon
founded by Kato N et al HCV-O.
A genome-length HCV RNA replication system may reflect the phenomenon
that HCV infected human liver undergoes.
Gastro Open J. 2016; 2(1): 9-13. doi: 10.17140/GOJ-2-125
