| Sumario: | Hepatitis C virus (HCV) replication is associated with
the endoplasmic reticulum, where the virus can induce
cellular stress. Oxidative cell damage plays an important
role in HCV physiopathology. Oxidative stress is triggered when the concentration of oxygen species in
the extracellular or intracellular environment exceeds
antioxidant defenses. Cells are protected and modulate
oxidative stress through the interplay of intracellular
antioxidant agents, mainly glutathione system (GSH)
and thioredoxin; and antioxidant enzyme systems such
as superoxide dismutase, catalase, GSH peroxidase,
and heme oxygenase-1. Also, the use of natural and
synthetic antioxidants (vitamin C and E, N-acetylcysteine, glycyrrhizin, polyenylphosphatidyl choline, mitoquinone, quercetin, S-adenosylmethionine and silymarin) has already shown promising results as co-adjuvants in HCV therapy. Despite all the available information, it is not known how different agents with antiviral activity can interfere with the modulation of the cell redox state induced by HCV and decrease viral replication. This review describes an evidence-based consensus on molecular mechanisms involved in HCV replication and their relationship with cell damage induced by oxidative stress generated by the virus itself and cell antiviral machinery. It also describes some molecules that modify the levels of oxidative stress in HCV-infected cells.
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