DIFFERENTIAL CONTRIBUTION OF HERPES-SIMPLEX VIRUS TYPE-1 GENE-PRODUCTS AND CELLULAR FACTORS TO THE ACTIVATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PROVIRUS

We have previously reported that infection with herpes simplex virus type 1 (HSV-1) activates expression of the human immunodeficiency virus type 1 (HIV-1) provirus in T cells. Activation of the HIV-1 provirus correlated with the activation of binding of 55- and 85-kDa proteins to the kappaB enhancer and binding of the 50-kDa HLP-1 protein to the LBP-1 sequences of the HIV-1 long terminal repeat. Further examination of this system has shown that the inhibition of HSV-1 replication by the antiviral drug acyclovir does not inhibit HSV-1-mediated induction of HIV-1 provirus. Surprisingly, the NF-kappaB and HLP-1 binding activities were substantially inhibited in acyclovir-treated cells. In the transient-transfection assay, ICP0, but not ICP4, activated the HIV-1 long terminal repeat promoter region and the effect of ICP0 was greatly enhanced in the presence of the NF-kappaB binding proteins, suggesting that induction of the HIV-1 provirus involves cooperation between the HSV-1-activated cellular factor, NF-kappaB, and the virus-encoded transactivator, ICP0.