Hepatitis C virus p7 induces mitochondrial depolarization of isolated liver mitochondria

You,Deok‑Gyun; Lee,Hye‑Ra; Kim,Won‑Ki; Kim,Hyung  Jung; Lee,Gi  Young; Yoo,Young  Do

doi:10.3892/mmr.2017.7809

Hepatitis C virus p7 induces mitochondrial depolarization of isolated liver mitochondria

Authors:
- Deok‑Gyun You
- Hye‑Ra Lee
- Won‑Ki Kim
- Hyung Jung Kim
- Gi Young Lee
- Young Do Yoo
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Affiliations: Laboratory of Molecular Cell Biology, Graduate School of Medicine, College of Medicine, Korea University, Seoul 02841, Republic of Korea, Department of Neuroscience, College of Medicine, Korea University, Seoul 02841, Republic of Korea, Department of Internal Medicine, Yonsei University College of Medicine, Yonsei University Health System, Seoul 03722, Republic of Korea
Published online on: October 17, 2017 https://doi.org/10.3892/mmr.2017.7809
Pages: 9533-9538

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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.

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