We observed an increase in expression of the chemotactic signaling receptor S1PR1 in HIV-infected thymic implants in humanized mice at 5 and 9 weeks post-infection, as well as in the thymus of systemically infected humanized mice at 12 weeks, which raises the critical question of whether upregulated S1PR1 translates to enhanced egress of functional thymocytes or, alternatively, a detrimental egress of less-functional naïve T cells due to more rapid intrathymic differentiation, as reported in studies of SIV-infected Rhesus macaques [27]. Here, S1PR1 is linked to infection.