Differential effects of human immunodeficiency virus type 1 envelope protein gp120 on interferon production by mononuclear cells from adults and neonates
Article
Nair, MPN, Chadha, KC, Stadler, I et al. (1995). Differential effects of human immunodeficiency virus type 1 envelope protein gp120 on interferon production by mononuclear cells from adults and neonates
. 2(4), 434-438. 10.1128/cdli.2.4.434-438.1995
Nair, MPN, Chadha, KC, Stadler, I et al. (1995). Differential effects of human immunodeficiency virus type 1 envelope protein gp120 on interferon production by mononuclear cells from adults and neonates
. 2(4), 434-438. 10.1128/cdli.2.4.434-438.1995
While considerable progress in examining the course of human immunodeficiency virus (HIV) infection in adults has been made, a better understanding of the natural history of perinatal HIV infection remains to be obtained. Dysregulation of the production and functions of various cytokines, especially the interferons (IFNs), during HIV infections has been reported. Using an in vitro model system, we examined the effects of the HIV type 1 envelope protein, gp120 (10, 50, and 100 ng ml), on gamma IFN (IFN-γ) and IFN-α production by lymphocytes from neonates and adults and also examined the potential regulatory effects of gp120 on phorbol 12-myristate acetate (PMA)- and Sendai virus-induced IFN-γ and IFN-α production by lymphocytes. PMA at a concentration of 50 ng/ml plus 50 ng of calcium ionophore A23187 per ml was used to induce IFN-γ, while 150 hemagglutinating units of Sendai virus was used to induce IFN-α production. The antiviral activity of both IFN-α and IFN-γ in leukocyte culture supernatants was assayed on BG-9 cells by a dye uptake technique using vesicular stomatitis virus as a challenge virus. Placental cord blood leukocyte (CBL) samples from healthy, term infants and adult peripheral blood leukocytes (APBL) produced no IFN in response to gp120. However, CBL produced significantly decreased levels of IFN-γ compared with APBL in response to PMA plus ionophore. gp120 significantly suppressed both Sendai virus-induced IFN-α and PMA-induced IFN-γ production by both CBL and APBL in a dose-dependent manner. However, gp120-induced suppression of IFN-α and IFN-γ was significantly greater with CBL than with APBL. Treatment of CBL and APBL with gp120 did not induce any phenotypic alteration of the CD45 RO+ subset. Increased suppression of IFN-α and IFN-γ production by gp120 in neonates may partially explain their apparent increased susceptibility to the clinical progression of HIV infections compared with that of adults.
