Depressive symptoms in patients with chronic hepatitis C are correlated with elevated plasma levels of interleukin-1β and tumor necrosis factor-α

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)-1β, IL-10 and tumor necrosis factor (TNF)-α]. t-Tests were performed to compare cytokine levels in patients with or without HCV. HCV patients showed higher TNF-α values compared to patients without HCV (group means = 7.94 vs. 3.41 pg/mL, respectively, p = 0.047). There were no significant differences between the groups for the other cytokines assessed. In patients with HCV, TNF-α and IL-1β 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.