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Abstract
Epidemiologists estimate hepatitis C viral infection (HCV) is the most common blood-borne viral infection in the United States and most of the western world. Pegylated interferon in combination with ribavirin is the standard of care for HCV. Though an effective pharmacological agent for HCV viral suppression, pegylated interferon induces neuropsychiatric side effects that culminate in a psychiatric disorder known as interferon induced major depressive disorder. Selective serotonin reuptake inhibitors (SSRIs) are widely used during HCV antiviral therapy to prevent or alleviate neuropsychiatric morbidity associated with pegylated interferon. However, it is unclear whether the anti-inflammatory properties of SSRIs inadvertently work against the pro-inflammatory properties of pegylated interferon in effect reducing the therapeutic efficacy of HCV antiviral therapy. The purpose of this study is to determine the effects of SSRIs and interferon induced major depressive disorder on sustained virological responses and quality of life in a cohort of HCV patients (n=46). Patients with active psychiatric disorders are included in the cohort. The study design is a longitudinal retrospective cohort design with a cross-sectional survey. Quantitative methods consist of an epidemiologic longitudinal analysis of a cohort of HCV patients who have previously undergone and completed pegylated interferon combination therapy. The measurements for the independent variables are SSRI use and interferon induced major depressive disorder, and HCV viral logs for the dependent variable. Generalized estimating equations (GEE) are used to determine the effects of SSRI therapy and interferon induced major depressive disorder on HCV viral logs over time. Qualitative methods consist of semi-structured interviews to compliment the quantitative findings. In this cohort, SSRI therapy and interferon induced major depressive disorder does not impact the probability of HCV patients achieving a sustained virological response. However, the mean slope of HCV viral logs decline faster over time in patients with interferon induced major depressive disorder in comparison to patients without interferon induced major depressive disorder (p=0.05). This finding suggests interferon induced major depressive disorder patients achieve sustained virological responses faster or suppress HCV viral replication more favorably over time during HCV antiviral therapy. Implications for treatment and management of HCV are discussed.