As in all retroviruses, there is a single promotor region in the LTR. This contains a variety of regulatory elements that respond to transcription factors (such as NF kappa b) produced by the host cell, thereby altering the rate of viral transcription. However, transcription is inefficient from this promotor. Tat, which is a viral protein that is encoded in three exons within the HIV genome, enhances transcription by enhancing processivity of RNA polymerase that copies the proviral DNA genome into genomic length RNA. Tat may also function to enhance transcription inhibition but more often the RNA is initiated and then terminates in a region of secondary structure giving rise to short RNA transcripts of 55-59 nucleotides. This region is in the TAT-responsive element (TAR). Why binding of TAT to TAR results in the greater processivity of the RNA polymerase is not known. TAT may also phosphorylate the C-terminal domain of RNA polymerase II, thereby rendering it more processive. Since the TAR region is in both the proviral DNA and in the genomic RNA transcript, TAT can bind to the latter as well; here is may bind to the nascent viral RNA and form part of the transcription complex

Curiously, during acute HIV infection, Tat is also secreted from infected cells (via a non-endoplasmic reticulum pathway similar to that used by bFGF and IL-1). This Tat can up-regulate HIV expression by neighboring infected cells and also has effects on Kaposi's sarcoma endothelial cells and other endothelial cells. Among other things, Tat causes these cells to express some metalloproteinases. The receptors for Tat are some of the integrins.

For further information see: Alan Frankel and John A. T. Young, HIV-1: Fifteen proteins and an RNA Annual Review of Biochemistry 67: 1-25, 1998