EVIDENCE THAT LEVELS OF THE DIMERIC CELLULAR TRANSCRIPTION FACTOR CP2PLAY LITTLE ROLE IN THE ACTIVATION OF THE HIV-1 LONG TERMINAL REPEAT IN-VIVO OR FOLLOWING SUPERINFECTION WITH HERPES-SIMPLEX VIRUS TYPE-1

The dimeric transcription factor CP2 binds a sequence element found ne ar the transcription start site of the human immunodeficiency virus (H IV-1) long terminal repeat. Several groups have suggested that cellula r factors binding this element might play a role in modulating HIV-1 p romoter activity in vivo. For example, induction of latent HIV-1 gene expression in response to superinfection by herpes simplex virus type 1 (HSV-1) or cytomegalovirus is thought to be mediated, in part, by fa ctors binding the CP2 site. In this report we began to examine directl y the relationship between CP2 and expression of the HIV-1 promoter. F irst, we tested what effect HSV-1 infection of T cells had on the cell ular levels of CP2. The results showed that HSV-1 infection led to a s ignificant reduction in the level of CP2 DNA binding activity and prot ein within 20 h. Next, we tested the effect of overexpressing either t he wild-type factor or a dominant negative variant of CP2 on HIV-1 pro moter activity in vivo. The results showed that CP2 had little effect or slightly repressed HIV-1 promoter activity in vivo. In addition, th ese expression constructs had little effect on the induction of HIV-1 promoter activity elicited by HSV-1 infection.