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1996-02-26
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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).