MODULATION OF HIV-LTR ACTIVITY BY RAS ONCOGENES

Cotransfection of NIH 3T3 cells with a mammalian expression vector con taining a v-Ha-rns gene, together with a plasmid carrying the human im munodeficiency virus (HIV) long terminal repeat (LTR) linked to the ch loramphenicol acetyl transferase (CAT) reporter gene, significantly st imulated CAT activity. High HIV LTR activation was also observed in ce ll lines carrying stably transfected ras oncogenes, activated by point mutation or amplification. By contrast an inactivated form of ras (Ha -ras Asn-17) did not stimulate the HIV-LTR but strongly inhibited its basal activity. Activation of the p21(ras) protein may thus be one of the signals that regulate LTR driven transcription during HIV infectio n.