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Updated: Feb 20, 2026
A Protocol for Analyzing Hepatitis C Virus Replication
Published on: June 26, 2014
Hepatitis C virus p7 induces mitochondrial depolarization of isolated liver mitochondria
Deok-Gyun You1, Hye-Ra Lee1, Won-Ki Kim2
1Laboratory of Molecular Cell Biology, Graduate School of Medicine, College of Medicine, Korea University, Seoul 02841, Republic of Korea.
Abstract:
Hepatitis C virus (HCV)‑encoded protein p7 is a viroporin that acts as an ion channel and is indispensable for HCV particle production. Although the main target of HCV p7 is the endoplasmic reticulum, it also targets mitochondria. HCV‑infected cells show mitochondrial depolarization and ATP depletion; however, the function of HCV p7 in mitochondria is not fully understood. The present study demonstrated that treatment of isolated mouse liver mitochondria with the synthesized HCV p7 protein induced mitochondrial dysfunction. It also demonstrated that HCV p7 targeted isolated mouse liver mitochondria and induced mitochondrial depolarization. In addition, HCV p7 triggered matrix acidification and, ultimately, a decrease in ATP synthesis in isolated mitochondria. These findings indicate that targeting of mitochondria by HCV p7 in infected cells causes mitochondrial dysfunction to support HCV particle production. The present study provided evidence for the role of HCV p7 in mitochondria, and may lead to the development of novel strategies for HCV therapy.
Insights
Hepatitis C virus p7 protein targets mitochondria, causing dysfunction and reduced ATP synthesis. This mitochondrial damage supports viral production and may offer new therapeutic targets for Hepatitis C.
Area of Science:
- Virology
- Mitochondrial Biology
- Biochemistry
Background:
- Hepatitis C virus (HCV) protein p7 is a viroporin essential for viral particle production.
- While primarily targeting the endoplasmic reticulum, HCV p7 also affects mitochondria, leading to depolarization and ATP depletion in infected cells.
- The precise role of HCV p7 within mitochondria remains unclear.
Purpose of the Study:
- To investigate the direct impact of Hepatitis C virus p7 protein on isolated mitochondria.
- To elucidate the mechanism by which HCV p7 induces mitochondrial dysfunction.
- To establish the role of mitochondrial targeting by HCV p7 in supporting viral replication.
Main Methods:
- Synthesis of Hepatitis C virus p7 protein.
- Treatment of isolated mouse liver mitochondria with synthesized HCV p7.
- Assessment of mitochondrial membrane potential, matrix pH, and ATP synthesis.
Main Results:
- HCV p7 protein directly targeted isolated mouse liver mitochondria.
- Treatment with HCV p7 induced mitochondrial depolarization and matrix acidification.
- HCV p7 significantly decreased ATP synthesis in isolated mitochondria, indicating impaired energy production.
Conclusions:
- HCV p7 protein directly induces mitochondrial dysfunction, including depolarization and impaired ATP synthesis.
- Mitochondrial targeting by HCV p7 plays a crucial role in supporting Hepatitis C virus particle production.
- These findings highlight mitochondria as a key target for developing novel Hepatitis C therapies.
