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Related Experiment Video

Updated: Jul 27, 2026

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Published on: July 16, 2012

Molecular dissection of hepatitis C virus expression.

S Okoshi¹, Y Takeda, M Takimoto

¹Third Department of Internal Medicine, Niigata University School of Medicine, Niigata, Japan. okoshi@med.niigata-u.ac.jp

|February 27, 2001

Summary

Hepatitis C virus 5' untranslated region (UTR) expression is controlled by cellular proteins. These proteins are present in adult mice and humans, but not in young mice, suggesting a role in viral gene regulation.

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Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis

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Published on: April 17, 2017

Area of Science:

Hepatology
Virology
Molecular Biology

Background:

The 5' untranslated region (5' UTR) of the hepatitis C virus (HCV) genome is crucial for viral gene expression.
The 5' UTR is a potential target for antiviral therapies.

Purpose of the Study:

To analyze the functional role of the HCV 5' UTR in vivo and in vitro.
To investigate the interaction of cellular proteins with the HCV 5' UTR.

Main Methods:

Generation of transgenic mice with a reporter gene containing the complete HCV 5' UTR.
Analysis of cellular protein binding to the 5' UTR using gel shift assays and affinity purification.
Comparison of protein-RNA complex formation in adult and young mice, as well as in human liver extracts.

Main Results:

Transgenic mice showed protein accumulation specifically in periportal hepatocytes.
Gel shift analysis revealed the presence of trans-acting proteins binding to a specific cis-acting element within the HCV 5' UTR in adult mice and humans, but not in young mice.
Evidence suggests these proteins recognize a stemmed RNA structure within the 5' UTR.

Conclusions:

Cellular factors regulate HCV 5' UTR expression in a tissue- and differentiation-specific manner.
The binding of specific proteins to the HCV 5' UTR is age-dependent in mice.
These findings highlight the importance of host-viral interactions in HCV replication and suggest potential therapeutic targets.