FIG 10.

Schematic illustration of p53-derived host restrictions against HIV-1 replication. HIV-1 provirus integration activates p53, followed by the induction of PKR. PKR phosphorylates Tat at least five Ser/Thr residues (T23, T40, S46, S62, and S68), which inhibits Tat function in three different ways: (i) phosphorylation near the ARM inhibits Tat translocation into the nucleus, (ii) Tat phosphorylation abolishes Tat-TAR binding, and (iii) Tat phosphorylation at T23 and/or T40 obliterates the Tat-cyclin T1 interaction.