ABSTRACT
The ACTGCTGA sequence (CTG motif) is located immediately upstream of the NF-kappaB enhancer in the human immunodeficiency virus type-1 (HIV-1) long terminal repeat (LTR). We previously reported on the frequent duplication of this motif in HIV-1-infected individuals. In this study we further characterized the role of the CTG element in transcription and its interaction with cellular proteins. We analyzed the biological activity of LTR promoters with dimeric, monomeric or deleted CTG motifs. Our results indicate that LTRs containing the monomeric CTG motif are the most active transcriptional promoters. Furthermore, mutant viruses with dimeric or deleted CTG motif were consistently out-competed by the wild-type virus in co-culture experiments. Gel mobility shift assays were used to identify a nuclear protein of approximately 68 kD that specifically interacts with this DNA sequence. Copyright 1994 S. Karger AG, Basel
