Notably, CD34+CD38- HSCs demonstrate elevated sensitivity to cell-cycle arrest following HTLV-1 infection in comparison to more mature CD34+CD38+ HPCs, suggesting that HTLV-1 may target stem cells to facilitate a latent infection in vivo by inducing cell cycle arrest to induce cellular quiescence (Figure 4). This evidence concerns the gene CD38 and disease arising from reactivation of latent virus.