Inhibition of adrenal cortical steroid formation by procaine is mediated by reduction of the cAMP-induced 3-hydroxy-3-methylglutaryl-coenzyme A reductase messenger ribonucleic acid levels.
Documented evidence supports the "cortisol connection' theory of acquired immune deficiency syndrome, linking glucocorticoid metabolism with immune function, and human immunodeficiency virus with them both. The peptide T subregion of gp 120 of human immunodeficiency virus apparently utilizes cellular melanocyte stimulating hormone receptors to competitively inhibit the blocking of interleukin-1 by melanocyte-stimulating hormone. Interleukin-1 stimulates CD8+ T-lymphocyte proliferation, as well as causing the release of corticotropin-releasing hormone, thereby stimulating the release of adrenocorticotrophic hormone and cortisol. Gp 120 also induces upregulation of adrenocorticotrophic hormone-related messenger ribonucleic acid. This apparently separate glucocorticoid metabolic route utilized by human immunodeficiency virus is the basis of the cortisol excess seen in human immunodeficiency virus infection. In vitro glucocorticoid-resistant lymphoid cells are resistant to human immunodeficiency virus infection as well. Viral resistance is also observed in patients who demonstrate glucocorticoid resistance. Glucocorticoid-responsive elements are contained in the human immunodeficiency virus (proviral and viral) genome that appear to regulate human immunodeficiency virus replication. Similarly, lymphoid-cell development and regulation depend on glucocorticoids. One may take advantage of this view of human immunodeficiency virus pathogenesis to create new methods of treatment.