HIV trans-activation response element (HIV TAR)

The **HIV trans-activation response element (TAR)** is a highly conserved, structured RNA element located at both the 5′ and 3′ ends of the HIV-1 RNA genome[1][3][9]. TAR forms a stem-loop (hairpin) structure of about 50 nucleotides and plays a central role in regulating HIV gene expression and replication. Its primary function is to serve as the binding site for the viral Tat (trans-activator of transcription) protein, which recruits the host transcription elongation machinery—most importantly, the positive transcription elongation factor b (P-TEFb)—to the HIV promoter, thereby stimulating efficient transcription of the viral genome[1][3][4][5][6][8]. The integrity of both bulge and loop regions is critical for function, with mutations in TAR resulting in severely impaired viral replication and gene expression[5]. In addition, TAR acts as a pre-microRNA, producing small viral RNAs that can modulate host gene expression to prevent apoptosis and reinforce viral latency[1][7]. TAR has also been shown to inhibit the host protein kinase R (PKR), thus enabling HIV to evade certain innate immune responses[3]. Due to its essential and multifaceted role in HIV biology, TAR is considered a therapeutic target, and significant effort has been placed on developing potent inhibitors—primarily small molecules, peptides, and peptide mimetics—that disrupt the Tat-TAR interaction, although none have advanced to clinical use yet[2][6].

Other names

Trans-activation response elementTAR elementHIV-1 TAR

Inhibition of Tat-TAR interaction to block viral transcription; Interruption of TAR-mediated protein recruitment (e.g., P-TEFb)