There is likely a complicated set of kinetics at play during HIV infection of the Thy/Liv implant in vivo, including but not limited to: the rate of viral replication and spread; the rate of induction of IFN-α in pDC; the rate of upregulation of CCR5 on thymocytes that express the IFN-α/β receptor; the rate at which these cells are infected and destroyed by R5 HIV; the rate at which they are replenished from earlier, CCR5− progenitors; and, not least, the rate at which more mature DP thymocytes are depleted. The gene discussed is IFNA2; the disease is HIV infectious disease.