Data reported in the literature show in the majority of cases an increased basal cortisol level in HIV-positive patients compared with controls, although the plasma concentration of cortisol in HIV-positive patients is generally within the physiological range. It is well known that pharmacological doses of glucocorticoids are immunosuppressive, but little is known about the effects of physiological concentrations of cortisol on the immune system. If a dialogue really exists between the HPA axis and the immune system, immune responses should be modulated by physiological concentrations of cortisol, as well as pathological levels of cortisol (high as in Cushing's syndrome or low as in Addison's disease), which are known to be associated with impaired immune system responses. We suggest that in HIV-positive patients, a chronic increase in the basal endogenous cortisol levels may provoke an imbalance in cytokine production, with a decrease in the production of type 1 and an increase in that of type 2. The type 1 to type 2 shift might be synergic with the increased cortisol levels in enhancing viral replication and apoptotic phenomena, and finally in causing the progression of HIV infection.
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