THE KINETICS OF HIV-1 LONG TERMINAL REPEAT TRANSCRIPTIONAL ACTIVATIONRESEMBLE THOSE OF HSP70 PROMOTER IN HEAT-SHOCK TREATED HELA-CELLS

The long terminal repeat (LTR) of human immunodeficiency virus type 1 (HIV-1) is activated under different conditions including heat shock. By using transient transfection assays, we have compared the thermal a ctivation of HIV-1 LTR to that of the promoter of the gene encoding th e human stress protein hsp70 which is under the control of the heat sh ock transcription factor HSF. In these assays, the chloramphenicol ace tyl transferase (Cat) gene was used as a reporter gene. Several parame ters of the heat stress were analyzed such as the temperature, the dur ation of heat stress and that of the recovery period. Under every cond ition tested, we have found that the kinetics of activation of both pr omoters were very similar. In addition, both showed a similar inhibiti on by actinomycin D. These results were compared to those obtained wit h a DNA construct containing the early promoter of SV-40 virus coupled to the Cat gene. In this case, no heat-mediated accumulation of CAT p rotein was observed, indicating that the transcriptional activation of HIV-1 LTR by heat shock is specific. HIV-1 LTR contains two NF-kappa B binding elements, involved in the activation of this promoter during oxidative stress, which are sequence related to the heat shock elemen t HSE. However, under all the heat shock conditions tested, we have be en unable to detect the binding of any protein to KB elements, suggest ing that this site is not directly involved in the thermal activation of HIV-1 LTR. These results indicate that the thermal transcriptional activation of HIV-1 LTR and hsp70 promoters occurs through different m echanisms that are triggered by similar heat shock conditions.