Persistence of the latent HIV reservoir is a major block to cure. The viral promotor, long terminal repeat (LTR), drives viral transcription and is enhanced by Transactivator of transcription (Tat). Inter- and intra- subtype LTR and tat genetic variation have shown to translate into functional differences. However, the effect of this genetic variation on viral latency development or reversal is unknown. Furthermore, the only HIV latency model available is subtype B based, referred to as JLAT. On the other hand, HIV-1C is responsible for approximately 46% of global HIV infections and is predominant in sub-Saharan Africa. Therefore, a minimal genome reporter virus for subtype C (termed “C731CC”) was constructed using HIV-1C consensus LTR and Tat. Jurkat cells were infected with C731CC to develop the JLAT C model of latency. The reactivation potential of HIV-1 subtype B and C was determined. We demonstrate that both subtypes express the same levels of Tat. Interestingly, HIV-1B was twice as more sensitive to stimulation with PMA, compared to subtype C suggesting that subtype C has a higher propensity for latency establishment than subtype B. Ongoing studies involve measuring the amount of integrated copies with Alu-gag PCR in both subtypes. We also replaced the consensus HIV-1C LTR and Tat in C731CC with patient-derived sequences and measured the reactivation potential of the different patient viruses with different latency reversing agents. We demonstrate that there was variable reactivation among these patient viruses, suggesting that the HIV-1 LTR could play a role in the propensity for latency establishment and/or reversal.