Endocrine, metabolic, and immunologic components of HIV infection

It is generally accepted that the progression of HIV infection is the consequence of increased HIV virus load and defective CD4+ T cell–mediated immunity. Previous studies have shown that T helper–directed cellular immunity is suppressed in hypercortisolemic HIV patients, while it is activated in cortisol‐resistant HIV patients. This is suggestive of a cytokine system intimately linked with cortisol and its receptors. Highly active antiretroviral therapy is an important advance in the treatment of HIV infection, but the suppression of viral replication is not associated with reconstitution of the immune function. This would account for reduced control of inflammation and the activation of 11β‐hydroxysteroid dehydrogenase type 1(11β‐HSD1) and increases in glucocorticoid and mineralocorticoid production in peripheral tissues. Such hormonal activation may cause insulin resistance and cardiometabolic complications. Therapeutic approaches with 11β‐HSD1 inhibitors, aldosterone antagonists, type 1 angiotensin receptor blockers, or renin inhibitors are suggested.