Neuropsychiatric Effects of Interferon Therapy in Chronic Hepatitis C
Summary
Interferon-α remains a cornerstone of antiviral therapy for chronic hepatitis C, yet its use is frequently complicated by neuropsychiatric symptoms. Up to half of treated patients experience depressive syndromes, anxiety, fatigue and cognitive slowing, leading to treatment discontinuation in many cases. These symptoms arise from peripheral immune activation and central inflammatory cascades. Interferon-α stimulates proinflammatory cytokines and activates indoleamine 2,3-dioxygenase, depleting tryptophan and shifting metabolism towards neurotoxic kynurenine metabolites. Excessive oxidative stress further impairs synaptic plasticity, particularly in the hippocampus, a region vital for mood regulation and memory. Genetic polymorphisms in cytokine or neurotransmitter pathways modulate individual susceptibility, while alterations in neurotrophic factors and glucocorticoid signalling contribute to neuronal atrophy and disrupted neurogenesis. Clinically, interferon-induced depression may persist after therapy, increasing the long-term risk of recurrent mood episodes. Early identification and combined management with antidepressant or anti-inflammatory agents can improve adherence and quality of life. Understanding these mechanisms offers insight into broader links between inflammation and psychiatric disorders and guides the development of safer antiviral regimens.
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Neuropsychiatric Effects of Interferon Therapy in Chronic Hepatitis C publication trend
The graph below shows the total number of articles in neuropsychiatric effects of interferon therapy in chronic hepatitis c across all publications each year (not limited to Nature Index journals).
Technical terms
Interferon-α: A type I interferon used as an antiviral and immunomodulatory agent in hepatitis C treatment.
Cytokines: Soluble proteins such as interleukins and tumour necrosis factor that mediate immune and inflammatory responses.
Neurogenesis: The process of generating new neurons from progenitor cells, principally in the hippocampus.
Hippocampus: A brain structure essential for learning, memory and emotional regulation, vulnerable to inflammatory and oxidative insult.
Indoleamine 2,3-dioxygenase (IDO): An enzyme activated by inflammation that degrades tryptophan into kynurenine, contributing to neurotoxicity and mood disturbances.
References
- Interferon therapy and its association with depressive disorders – A review. Frontiers in Immunology (2023).
- Interferon-Alpha Reduces Human Hippocampal Neurogenesis and Increases Apoptosis via Activation of Distinct STAT1-Dependent Mechanisms. The International Journal of Neuropsychopharmacology (2017).
- The role of circulatory systemic environment in predicting interferon-alpha–induced depression: The neurogenic process as a potential mechanism. Brain Behavior and Immunity (2019).
- Recurrence of depressive disorders after interferon-induced depression. Translational Psychiatry (2017).
- Glucocorticoid Receptors, Brain-Derived Neurotrophic Factor, Serotonin and Dopamine Neurotransmission are Associated with Interferon-Induced Depression. The International Journal of Neuropsychopharmacology (2015).
- Toward an Anti-Inflammatory Strategy for Depression. Frontiers in Behavioral Neuroscience (2011).
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