Human immunodeficiency virus type-1 (HIV-1) replication and pro viral gene expression are exquisitely responsive to factors that induce cellular stress. Oxidants, ultraviolet (UV) light, osmotic stress, heat shock and pro-inflammatory cytokines all promote proviral gene expression and enhance viral proliferation (1 –6 ). In quiescent or unstimulated cells, the HIV-1 promoter exhibits a low basal level of transcriptional activity that can be activated 12- to 150-fold following exposure to a mitogenic or stress-inducing stimulus (3 ,6 ). This dramatic induction of transcription is achieved by integrating a complex network of cellular signal-transduction pathways, with a variety of highly responsive transcription factors that bind to and modulate the transcriptional activity of the viral promoter. Therefore, not only is the viral promoter highly responsive to diverse physiological stimuli, but this transcriptional activity is correlated directly with the activation status of specific kinase-regulated signal transduc-tion pathways (6 ,7 ).
