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Salicylic Acid Inhibits Ultraviolet- and cis-Platinum-induced Human Immunodeficiency Virus Expression¹

Center for Mechanistic Biology and Biotechnology, Argonne National Laboratory, Argonne, Illinois 60439-4833 [G. E. W., S. S.], and Departments of Pathology [G. E. W., J. P., C. R. L.] and Medicine [C. R. L.], Loyola University Medical Center, Maywood, Illinois 60154

Previous studies have shown that exposure of HeLa cells stably transfected with an HIV-long terminal repeat-chloramphenicol acetyltransferase (HIV-LTR-CAT) construct to many DNA-damaging agents (such as UV light) induces expression from the HIV LTR. By culturing the cells with salicylic acid we demonstrated dose-dependent repression of this UV- or cis-platinum (cis-Pt)-induced HIV expression. While salicylic acid treatment, indomethacin treatment, UV exposure, or cis-Pt treatment alone decreased viability by up to 50%, equal numbers of viable cells were used for the CAT assays. Repression was evident if salicylic acid was administered 2 h before, at the same time as, or up to 6 h after exposure to the DNA-damaging agent. The kinetics were similar for UV- and for cis-Pt-induced HIV expression, and induction was dependent on the UV dose or cis-Pt concentration added to the culture. pH changes of the media alone in the absence of salicylic acid did not affect HIV expression. Indomethacin (100 µM) did not affect UV- or cis-Pt-induced HIV expression. These results suggest a role for the prostaglandins or the cyclooxygenase pathway or both in HIV induction mediated by DNA-damaging agents.

¹ This work was supported by the United States Department of Energy, Office of Health and Environmental Research Contract W-31-109-ENG-38.

² To whom requests for reprints should be addressed, at Center for Mechanistic Biology and Biotechnology, Argonne National Laboratory, 9700 South Cass Avenue, Argonne, IL 60439-4833.

³ Present address: Department of Chemistry, University of South Carolina, Columbia, SC 29208.

Received 8/ 2/94. Accepted 2/14/95.