       Document 0297
 DOCN  M9620297
 TI    HIV and the cortisol connection: a feasible concept of the process of
       AIDS.
 DT    9602
 AU    Corley PA
 SO    Med Hypotheses. 1995 Jun;44(6):483-9. Unique Identifier : AIDSLINE
       MED/96038373
 AB    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.
 DE    Acquired Immunodeficiency Syndrome/*PHYSIOPATHOLOGY  Ascorbic
       Acid/PHARMACOLOGY/THERAPEUTIC USE  Corticotropin/PHYSIOLOGY  Genome,
       Viral  Glucocorticoids/BIOSYNTHESIS/PHYSIOLOGY  Human
       Hydrocortisone/PHARMACOLOGY/*PHYSIOLOGY
       HIV/GENETICS/*PHYSIOLOGY/*PATHOGENICITY
       HIV-1/GENETICS/PHYSIOLOGY/PATHOGENICITY  Lupus Erythematosus,
       Systemic/PHYSIOPATHOLOGY  Models, Biological  Pituitary
       Hormones/PHYSIOLOGY  Receptors, Glucocorticoid/PHYSIOLOGY  Virus
       Replication/DRUG EFFECTS  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

