title: HIV and the cortisol connection: a feasible concept of the process of AIDS.
abstract: Recent evidence suggests that HIV infection and the clinical and laboratory manifestations of acquired immunodeficiency syndrome (AIDS) are a result of the genetic influence of the virus on cellular adrenocorticotrophic hormone (ACTH) and cortisol metabolism. Recent genetic studies substantiate this view with the observation that the HIV-1 genome is linked to glucocorticoid inducibility and to glucocorticoid receptor binding, and may explain the strong ability of cortisol to enhance HIV replication. Adrenocortical hyperactivity observed in HIV-infected individuals has been found to be independent of the hypothalamic-pituitary axis, and is apparently a result of increased ACTH production by HIV. It is proposed that the HIV-induced cortisol excess is the foundation of the immunosuppression seen in AIDS, and is the basis for alternative avenues of treatment, including the use of ascorbic acid.
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone / Q000502:physiology; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use; D016679:Genome, Viral; D005938:Glucocorticoids / Q000096:biosynthesis / Q000502:physiology; D006678:HIV / Q000235:genetics / Q000472:pathogenicity* / Q000502:physiology*; D015497:HIV-1 / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology / Q000502:physiology*; D008180:Lupus Erythematosus, Systemic / Q000503:physiopathology; D008954:Models, Biological; D010907:Pituitary Hormones / Q000502:physiology; D011965:Receptors, Glucocorticoid / Q000502:physiology; D014779:Virus Replication / Q000187:drug effects
chemical_list: D005938:Glucocorticoids; D010907:Pituitary Hormones; D011965:Receptors, Glucocorticoid; D000324:Adrenocorticotropic Hormone; D001205:Ascorbic Acid; D006854:Hydrocortisone