ACTIVATION OF THE HIV TYPE-1 LONG TERMINAL REPEAT AND VIRAL REPLICATION BY DIMETHYLSULFOXIDE AND RELATED SOLVENTS

The HIV-1 long terminal repeat (LTR) introduced into the macrophage ce ll line THP-1 and the T lymphocyte cell line Jurkat in association wit h the luciferase reporter gene is activated by the polar, aprotic solv ents dimethylsulfoxide (DMSO), dimethylacetamide (DMAC), and dimethylf ormamide (DMF). These solvents also greatly potentiated the activation of the LTR in THP-1 cells by phorbol myristate acetate (PMA), tumor n ecrosis factor alpha (TNF-alpha), H2O2, and a Staphylococcus epidermid is product. Lipopolysaccharide (LPS) and lipoteichoic acid (LTA) at 1 mu g/ml had no effect on the LTR in THP-1 cells unless the solvents we re added. The aprotic solvents also greatly potentiated the activation of the LTR in Jurkat cells by PMA, TNF-alpha, and H2O2, whereas LPS, LTA, or the S. epidermidis product had no effect in the presence or ab sence of the solvents. DMSO, DMAC, and DMF also increased the producti on of intact virions by latently HIV-1-infected ACH-2, J1.1, U1, and O M10.1 cells under some experimental conditions. The use of the polar a protic solvents DMSO, DMAC, and DMF, by amplification, may allow the b etter detection of a weak activator of the LTR and facilitate studies of the mechanism of activation.