Fluoxetine as a Novel Hepatitis C Treatment

the MPR take:

Adding the selective serotonin reuptake inhibitor (SSRI) fluoxetine to interferon (IFN)-alpha-based therapy in patients with chronic hepatitis C (CHC) may not only reduce IFN-alpha-therapy-related depression but may also improve the  anti-HCV treatment, says a new study published in the journal Antiviral Research. Previous studies have shown that SSRIs alter hepatic lipid biosynthesis, have anti-inflammatory properties, negatively affect MAPK or STAT-1 signals, act as suppressors to infectivity and replication of human immunodeficiency virus (HIV), and are potent inhibitors of enterovirus replication. A new study has found that fluoxetine has the ability to inhibit hepatitis C virus (HCV) infection by either activating PPAR-beta/gamma or by strengthening IFN-alpha-mediated activations of JNK/STAT-1; this in turn reduces hepatic pathogenesis including reactive oxygen species production and lipid accumulation. Because of these synergistic effects, the authors suggest reducing the doses of fluoxetine and INF-alpha to improve the efficacy of anti-HCV treatment and decrease the chance of adverse effects.

More than 20% of chronic hepatitis C (CHC) patients receiving interferon-alpha (IFN-α)-based anti-hepatitis C virus (HCV) therapy experienced significant depression, which was relieved by treatment with fluoxetine. However, whether and how fluoxetine affected directly the anti-HCV therapy remained unclear.

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