After the entry of the virus, the capsid frees viral RNA into the cytoplasm. This is by all accounts regulated by T-cell receptor-interacting molecule 5, a protein that may limit viral replication by repressing the amount of capsid, which can be freed into the cytoplasm (Arhel, 2010; Pertel et al., 2011). Two molecules of the viral genomic RNA and different proteins that are required for replication and integration are found in the viral capsid.

The viral polymerase executes the Reverse transcription. Reverse transcriptase, equipped for using two distinct templates. At first it uses the genomic viral RNA to synthesize a single stranded DNA, then reverse transcriptase uses it as a template to synthesize a double-stranded DNA (dsDNA) (Fig. 1) (Zucker et al., 2001). The viral genomic RNA by the activity of RNase is degraded which is presented in the reverse transcriptase enzyme, subsequently permitting the sdDNA molecule to be used for dsDNA synthesis as a template (Zucker et al., 2001).

Afterwards of the reverse transcription, viral double-stranded DNA is associated in the preintegration complex. It is known that the preintegration complex is flexible and that its viral and cellular protein composition differs during its way toward the nucleus (Arhel, 2010). The transportation of the reintegration complex to the nuclear membrane is considered to be interceded through the TNPO3 nuclear pore (Zaitseva et al., 2009; Arhel, 2010; Ocwieja et al., 2011). As soon as in the nucleus, the viral DNA is fastened to the chromatin by the activity of a cell protein, lens epithelium-inferred development variable/p75 (Van Maele et al., 2006). In spite of the fact that integration happens at random process in the cell genome, it has been demonstrated that HIV DNA is fastened to less condensed chromatin region (Brady et al., 2009; Ocwieja et al., 2011).