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Published on: November 17, 2018
Interplay between Hepatitis C Virus and Redox Cell Signaling
Anna Ruggieri1, Simona Anticoli, Lucia Nencioni
1Department of Infectious, Parasitic and Immune Mediated Diseases, Italian National Institute of Health, 00161 Rome, Italy. anna.ruggieri@iss.it.
Insights
Hepatitis C virus (HCV) infection impacts global health. This review explores how oxidative stress influences HCV replication and identifies host cell pathways as potential therapeutic targets for new treatments.
Area of Science:
- Hepatology
- Virology
- Cellular Biology
Background:
- Hepatitis C virus (HCV) infection affects 3% of the global population.
- Current treatments for chronic HCV infection have limitations in efficacy and tolerability.
- Novel therapeutic strategies targeting host cell pathways are needed.
Purpose of the Study:
- To review the impact of oxidative stress on the HCV life cycle.
- To identify key redox-regulated intracellular pathways involved in HCV replication.
Main Methods:
- Literature review of studies on oxidative stress and HCV.
- Analysis of host cell signaling pathways modulated by HCV.
- Examination of the dual role of oxidative stress in viral replication.
Main Results:
- HCV manipulates host cell redox-regulated pathways for replication.
- Oxidative stress induced by HCV affects viral replication, disease progression, and severity.
- The precise role of oxidative conditions in HCV replication is complex, showing both positive and negative effects.
Conclusions:
- Understanding the interplay between oxidative stress and HCV is crucial for developing new therapies.
- Targeting host cell redox pathways presents a promising strategy for novel anti-HCV drug discovery.
- Further research into redox-regulated pathways could lead to more effective treatments for chronic HCV infection.
Abstract:
Hepatitis C virus (HCV) infects approximately 3% of the world's population. Currently licensed treatment of HCV chronic infection with pegylated-interferon-α and ribavirin, is not fully effective against all HCV genotypes and is associated to severe side effects. Thus, development of novel therapeutics and identification of new targets for treatment of HCV infection is necessary. Current opinion is orienting to target antiviral drug discovery to the host cell pathways on which the virus relies, instead of against viral structures. Many intracellular signaling pathways manipulated by HCV for its own replication are finely regulated by the oxido-reductive (redox) state of the host cell. At the same time, HCV induces oxidative stress that has been found to affect both virus replication as well as progression and severity of HCV infection. A dual role, positive or negative, for the host cell oxidized conditions on HCV replication has been reported so far. This review examines current information about the effect of oxidative stress on HCV life cycle and the main redox-regulated intracellular pathways activated during HCV infection and involved in its replication.
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