Abstract
The effects of ascorbate (vitamin C) and azidothymidine (AZT) were examined on HIV expression in permanently infected and reporter cell lines. In T-lymphocytic HXB cells, constitutively producing moderate to high levels of virus, ascorbate suppressed HIV production and reduced the yield of infectious virus released into the culture supernatant. AZT, which has been reported to block de novo infection of freshly infected cells, did not inhibit constitutive virus production in HXB cells. In latently infected ACH-2 T-cells, producing low basal level of virus, exposure to phorbol ester (PMA) caused about 10-fold increase in virus production. Pre-treatment of ACH-2 cells with ascorbate followed by PMA stimulation resulted in a dose-dependent reduction in the extracellular level of HIV reverse transcriptase activity. AZT treatment did not suppress HIV activation in PMA-stimulated ACH-2 cells. In mixed cultures of uninfected HLCD4-CAT and infected HL2/3 cells, ascorbate did not affect virus-induced (taX-mediated) transcriptional activation of the CAT reporter gene linked to the HIV long terminal repeat. These results reveal anti-HIV effects of ascorbate that offer potential for development of combined therapy with other agents.