INTERACTIONS BETWEEN HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION AND HORMONAL PATHWAYS - ENHANCEMENT OF CALCIUM-INDUCED BUT REDUCTION OF GLUCOCORTICOID-INDUCED CELL-DEATH

We examined the effect of chronic human immunodeficiency virus 1 (HIV- 1) infection on the growth of human leukemic CEM T cells, exposed to c ompounds which act through several major hormone or hormone-like signa l transduction systems. Three were not altered by HIV-1 infection. Mic romolar 8-bromo-cAMP inhibited cell growth equally in uninfected and i nfected cells. At the concentrations tested, neither (Bu)gcAMP nor the stimulator of protein kinase C, phorbol 12-myristate 13-acetate, alte red the growth of infected or uninfected cells. The synthetic prostagl andin analog enisoprost also inhibited both equally. However, response s to two basic signal transduction systems, calcium uptake and the glu cocorticoid pathway, were influenced by HIV infection. In chronically HIV-infected cells increased sensitivity to lysis by the calcium ionop hore A23187 was observed. Additionally, the infected cells contained r educed amounts of glucocorticoid receptor sites and showed a statistic ally significant shift toward resistance to glucocorticoid-induced apo ptosis.