White blood cells and extracellular fluid from HIV infected individuals have been shown to be deficient in reduced glutathione (GSH). GSH is the most abundant intracellular thiol and serves as an antioxidant, protecting cells from endogenous and exogenous toxic compounds as well as ionizing radiation and oxidative stress. Procysteine (L-2-oxothiazolidine-4-carboxylic acid) is actively transported across cell membranes into the cytoplasm where it is metabolized to L-cysteine, a key rate limiting component in the formation of GSH. Extracellular procysteine appears to be less toxic than either cysteine or N-acetyl cysteine, two other drugs used to increase intracellular GSH. We report that procysteine inhibits the upregulation of HIV production in TNF-alpha stimulated U1 cells. In several experiments, p24 was suppressed in a dose related manner, with 1, 5, and 10 mM procysteine reducing TNF-alpha induced production by 0-30, 35-70, and 60-80%, respectively. At these concentrations procysteine had no significant effect on cell viability, or proliferation after one week of treatment.

*HIV/DRUG EFFECTS *Thiazoles/PHARMACOLOGY *Tumor Necrosis Factor/PHARMACOLOGY *Virus Replication/DRUG EFFECTS

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