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The Trans-activation response element of HIV-1 (TAR) is a highly conserved 59-nucleotide RNA stem-loop at the 5′ end of HIV-1 mRNAs. It is essential for efficient transcriptional elongation of viral genes by serving as a binding site for the viral Tat protein and host factors (such as cyclin T1 and CDK9), which recruit and stabilize RNA polymerase II on the viral promoter.[5][3][1] The TAR element’s interaction with Tat dramatically increases the levels of viral transcripts required for HIV-1 replication. Structural details, such as the UCU bulge and loop, are critical for Tat recognition and binding, and disruption of this interaction strongly inhibits viral replication.[5] TAR RNA can also produce viral microRNAs that modulate host cell processes, such as apoptosis, and may play a role in the viral life cycle and pathogenesis.[3][1] TAR is actively studied as a potential therapeutic target to block HIV-1 gene expression.
Inhibition of Tat–TAR binding, thereby blocking HIV-1 transcriptional activation; Modulation of RNA structure or stability to impair viral gene expression.
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