Trans-activation response element (TAR)

The trans-activation response element (TAR) is a structured RNA hairpin located at the 5′ end of all nascent HIV transcripts, critical for the recruitment of the viral Tat protein. Upon Tat binding, P-TEFb is recruited, leading to phosphorylation of RNA polymerase II and transition from transcriptional pausing to processive elongation, which is absolutely essential for HIV replication[3][4][9]. The TAR–Tat–P-TEFb axis is a central regulator of the HIV lifecycle and a unique drug target, as disruption prevents viral gene expression and replication. While the TAR element itself is not a conventional receptor, enzyme, or protein target, it does serve as the necessary substrate for Tat-directed transactivation and is being explored as an antiviral therapeutic target in research, primarily to disrupt the Tat–TAR–P-TEFb interaction[2][4][9][10]. Structurally, TAR forms a stem-loop motif required for complex assembly, and its sequence and conformation can influence susceptibility to inhibitors and viral fitness[3][6][7].

Other names

TAR elementHIV TARTrans-activation response (TAR) element

For experimental drugs: Blockade or disruption of Tat–TAR RNA binding, inhibiting HIV transcriptional activation and viral replication