CCR5 and infection: In summary, our model predicts that post-ATI viral control during autologous HSPC transplantation is obtained when (1) the transplanted HSPC dose is significantly higher than the residual endogenous HSPCs that persist through myeloablative conditioning (in this case TBI) and (2) the fraction of protected (i.e. CCR5-edited) HSPCs in the transplant (fp) is sufficiently high to outcompete cells susceptible to infection and disrupt ongoing cycles of viral replication.