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Studies suggest that cytokines have a role in the biology of depression. In this study, we evaluated depression and cytokine levels in patients with and without chronic hepatitis C (HCV) to better assess how chronic infection alters cytokines levels and may contribute to depressive symptomotology. Twenty-three adults with (n=16) and without (n=7) HCV were recruited through the Portland VA Medical Center. Research participants were excluded for current substance abuse, psychotic disorder, liver cirrhosis, or interferon (IFN) therapy. Participants completed the Beck Depression Inventory-II (BDI-II) and a blood draw to evaluate plasma cytokine levels [i.e., interleukin (IL)-1beta, IL-10 and tumor necrosis factor (TNF)-alpha]. t-Tests were performed to compare cytokine levels in patients with or without HCV. HCV patients showed higher TNF-alpha values compared to patients without HCV (group means=7.94 vs. 3.41pg/mL, respectively, p=0.047). There were no significant differences between the groups for the other cytokines assessed. In patients with HCV, TNF-alpha and IL-1beta levels (but not IL-10) were correlated with BDI-II scores [r=0.594, p=0.020 and r=0.489, p=0.055 (trend), respectively]. Taken together, these results show an association between severity of depressive symptoms and expression of pro-inflammatory cytokines in patients with HCV. Future studies should investigate how inflammatory mediators play a role in the expression of specific depressive symptoms in patients with chronic infection. Patients with HCV represent an interesting model to examine this relationship.

Thirty-nine patients with hepatitis C viral infection on interferon-alpha (IFN-alpha) therapy were monitored weekly using the Beck Depression Inventory (BDI). Thirteen of thirty-nine patients (33%) developed IFN-alpha-induced major depressive disorder (MDD). During the course of IFN-alpha therapy, patients who became depressed were treated with citalopram, a selective serotonin reuptake inhibitor (SSRI) antidepressant. Results indicated that: (1) IFN-alpha response rates were significantly higher in those patients who developed IFN-alpha-induced MDD than in those who did not (end-of-treatment response (ETR) rates: 61.5% versus 26.9% and sustained viral response (SVR) rates: 38.5% versus 11.5%), (2) male patients with ETR to IFN-alpha therapy were, on average, approximately 33 pounds lighter in body weight than male patients who did not respond, and (3) gender, race, past history of MDD, and past history of substance abuse were not significantly associated with ETR. In conclusion, our findings suggest that IFN-alpha-induced MDD may be a predictor of a positive response to IFN-alpha therapy, or an indication of optimal dosing.