Gene expression of human immunodeficiency virus (HIV-1) is greatly enh
anced by a viral transactivator, the Tat protein, which interacts with
R region sequences' of the HIV-1 long terminal repeat (LTR). There is
no direct evidence to indicate transcriptional activation of HIV-1 by
Tat. Using an in vitro transcription system, we demonstrate that an e
stablished mouse cell line, which constitutively expresses Tat protein
, selectively stimulates the steady state levels of the transcripts di
rected from the Long terminal repeat (LTR) sequences of HIV-1. The gel
binding retardation assays further demonstrate a stable activated com
plex, formed due to direct binding of Tat to DNA elements of the HIV-1
LTR. These data implicate transcription as the site of Tat action in
trans-activation and could play an essential role in human immunodefic
iency virus replication, similar to the nuclear trans-activators of ot
her viruses.