HIV, depression and compliance: the mediating role of cytokines. A review of the international literature

Abstract

HIV-positive individuals are at greater risk of depression, which is known to influence their well-being negatively. In fact, depression may promote unhealthy behaviors (e.g. drug use and intentional unprotected sex); furthermore, depression may also act reducing immune system functioning. However, the relationship between the immune system and depression is bidirectional, since many physchoneuroimmunological research studies have shown that immune system activation, more specifically pro-inflammatory cytokines, increases the risk of depression. Thus, HIV-positive persons with co-infection (e.g. HCV), taking HAART and/or interferon-α, may show cytokine dysregulation. This may explain the greater prevalence of depression among HIV-positive individuals. In fact, pro-inflammatory cytokines and cortisol (also known as stress hormone), both promote tryptophan depletion, which is commonly associated with depressive symptoms. Hence, depression may negatively influence compliance, increasing the risk for incorrect assumption of antiretroviral leading to a significant reduction of immune system functioning. This review examines the relationship between HIV infection, co-infection (e.g., HCV), HAART and/or interferon-α therapy and cytokine dysregulation, with a focus on the influence of pro-inflammatory cytokines in promoting depression, which could ultimately reduce compliance. Evidence-based pharmacological and psycho-social interventions on depression are also discussed.