Together, these results suggest that enrichment for latent infection in the non-dividing cell subpopulation cannot be attributed to the inhibitory effect of Vpr on cell cycle progression, but rather is more likely due to increased overall expression of HIV accessory proteins during productive wild type virus infection, especially those linked to apoptotic induced cell death (i.e. Vpr, Tat, Nef) [43]. The gene discussed is S100B; the disease is disease arising from reactivation of latent virus.