Human immunodeficiency virus induction of corticotropin in lymphoid cells

Disruption of the linkage among the immune, nervous, and endocrine systems may contribute to the pathology and symptoms of acquired immunodeficiency s yndrome (AIDS). We investigated the role of human immunodeficiency virus (H IV) in altering these linkages via induction of corticotropin (ACTH) by lym phocytes. Cultured T lymphocytes (119 cell line) were infected with HIV-1, after which ACTH production was measured and characterized at Various time intervals by immunofluorescence and Western blotting. We report a coordinat e expression of ACTH and p24 HIV core protein in 119 cells. Also, the kinet ics of HIV-induced ACTH production by 119 T lymphoma cells are demonstrated using three different strains of HIV as well as UV-inactivated HIV. ACTH p roduction corresponded with the appearance of p24 antigen and was maximal 3 5 days after infection. UV-inactivated HIV and the viral envelope protein, gp120, were also able to induce ACTH production in these cells, indicating that viral replication was not required for the ACTH induction. The HIV-ind uced ACTH was synthesized de novo and had the size and biological activity of pituitary ACTH. Inhibition of ACTH in HIV-infected lymphocyte cultures b y anti-ACTH antiserum enhanced viral p24 expression. The significance of ly mphocyte ACTH in AIDS is not clear, but these results suggest that it may r estrict HIV replication and possibly infection.