Important note: Information in this article was accurate in 1993. The state of the art may have changed since the publication date.
Interferon-gamma-activated monocytes impair infectivity of HIV particles by an oxygen metabolite-dependent reaction.
Int Conf AIDS. 1993 Jun 6-11;9(1):171 (abstract no. PO-A13-0222). Unique Identifier : AIDSLINE MED/93333654 Ennen J; Kurth R; Paul-Ehrlich Institut, Langen, Germany.
Abstract:
Mononuclear phagocytes generate microbicidal oxygen metabolites spontaneously and after phagocytic stimulation by a NADPH-dependent enzymatic reaction called the oxidative burst. The spontaneous release of reactive oxygen radicals and intermediates (ROI) increases five to eight-fold after treatment of monocytes with the lymphokine interferon-gamma (IFN-gamma). The effect of the IFN-gamma activated release of ROI by human monocytes on the infectivity of free human immunodeficiency virus HIV) in the supernatant was investigated with the following results: First, IFN-gamma activated but neither control monocytes nor lipopolysaccharide stimulated monocytes effectively decreased the infectivity of cell-free HIV-1 in culture medium supernatant. Second, the mechanism of inactivation was dependent on the enhanced spontaneous release of ROI by IFN-gamma activated mononuclear phagocytes since the enzyme catalase or the free radical scavenger butylated hydroxyanisol (BHA) could block this activity. Third, soluble and solid-phase HIV-1 outer envelope glycoprotein (gp120) failed to trigger the oxidative burst activity after specific gp120-monocytic CD4 receptor interaction. These results indicate an anti-viral effect of interferon-gamma-activated monocytes/macrophages on HIV-1 which may have important implications for our understanding of the spread of the virus in the body and the development of full-blown AIDS after a long period of latency.
Keywords: *HIV-1/DRUG EFFECTS *Interferon Type II/PHARMACOLOGY *Monocytes/DRUG EFFECTS 931130
M93B5439
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