Abstract
Similarly to HIV-infected cells, recombinant HIV-1 glycoprotein 120 induces acid-labile interferon production in peripheral blood mononuclear cells from healthy donors. Acid lability of this interferon is due to the presence of both IFN-α and -γ molecules. In fact, although not revealed by neutralization of antiviral activity with antibody to IFN-γ, the presence of IFN-γ was shown both immunoenzymatically and by detection of specific mRNA in gp120-stimulated cells. The source of IFN-γ appears to be a T cell present in the CD4-enriched subpopulation. Cultures treated with monoclonal antibodies to the ICAM-1 and LFA-1 adhesion molecules showed an impaired release of both IFN types after gp120 stimulation, suggesting a crucial role of cell-to-cell interactions in the process leading to IFN production.
Our data suggest that the HIV envelope glycoprotein could be responsible for the induction of endogenous IFN-α and -γ observed in AIDS patients.
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