Trans-activation response element of human immunodeficiency virus RNA (TAR element)

The **Trans-activation response (TAR) element of HIV RNA** is a highly conserved structured RNA hairpin present at the 5′ and 3′ ends of all HIV-1 transcripts[1][2][3][4][5]. It primarily functions as an essential regulatory switch, binding the viral Tat protein to enhance the processivity of RNA polymerase II at the HIV long terminal repeat (LTR) promoter, greatly increasing transcription of the viral genome[1][2][4][5]. Besides its primary transcriptional regulatory role, TAR is involved in multiple steps of the HIV lifecycle, including regulating translation (repression), promoting genome packaging, participating in reverse transcription, and acting as an inhibitor of the host antiviral PKR protein[1][3]. TAR RNA can also be processed by Dicer to generate a microRNA-like molecule, potentially contributing to viral latency and suppression of apoptosis in infected cells[5][6]. Its essential and multifaceted nature makes it an attractive, though technically challenging, target for antiviral drug development[1][5][6].

Other names

HIV TARTAR RNAHIV-1 TARHIV-1 TAR RNATrans-activation response element

Inhibition of Tat–TAR interaction blocks transcriptional elongation in HIV, suppressing viral replication[1][2][5]. Small molecules, oligonucleotides or other ligands may bind TAR RNA, preventing Tat binding or altering RNA structure to inhibit function[1].