Figure 1. Different phases of HIV transcription.

A), The binding of NF-κB and NF-AT to the enhancer region of HIV LTR strongly upregulates the initiation phase of HIV transcription. The histone acetyl transferases (HATs) recruited by these factors, catalyze the acetylation of core histones and establish the transcriptionally active chromatin (euchromatin) structures. The establishment of euchromatin structures at and around LTR promoter promotes efficient access of LTR to transcription machinery. Transcriptional initiation is characterized by the phosphorylation of serine residues at position 5 (S5) in the heptapeptide (YSPTSPS)₅₂ repeats of the C-terminal domain (CTD) of RNAPII by TFIIH/Cdk7. B), HIV transcription halts after passing through the TAR elements due to the binding of negative transcriptional elongation factors, mainly NELF and DSIF. C), Tat protein of HIV brings the super elongation complex (SEC), containing P-TEFb at HIV LTR along with it. The CDK9 subunit of P-TEFb subsequently catalyzes the phosphorylation of negative elongation factors DSIF and NELF, which leads to either their dissociation from LTR or reverse their function from negative to positive elongation factor. CDK9 also catalyzes the phosphorylation of CTD of RNAPII, primarily at serine 2 residues. This event makes RNAPII highly processive or transcription elongation proficient that result in the generation of complete and properly processed HIV transcripts.