Figure 3.

A model of post-integration latency in HIV-1-infected microglia. Post-integration latency is manifested through several mechanisms, including chromatin remodeling, epigenetic mechanisms, and host-encoded miRNAs. Histone deacetylase 1 (HDAC1) causes chromatin remodeling, which is responsible for the inhibition of HIV-1 gene expression. C-promoter binding factor-1 (CBF-1) and COUP-TF-interacting protein 2 (CTIP2) have also been implicated in the recruitment of HDACs to the pr-oviral promoter, thereby establishing latency. Moreover, Tat can mediate reactivation of this process. Integrated HIV-1 pro-viral DNA is also delimited at both ends by the HIV-1 LTR. The 5′ LTR has unique blend of a robust TATA box, a potent initiator sequence, and binding sites for several TFs, including the glucocorticoid receptor COUP, upstream stimulatory factor (USF), activator protein 1 (AP1), TCF-1α, C-Myc, specificity protein 1 (SP1), CTF/NFE, nuclear factor of activated T cells (NFAT), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κβ), and Tat.