This may be partly because of the active role of thymus in children in the development of mature T lymphocytes, while the thymic microenvironment further enhances the CXCR4 tropism of thymocytes (82) Recent reports showed, using humanized mouse models, that infection with CCR5-tropic HIV-1 strains may result in depletion of bone marrow CD34+ cells, which was dependent on the presence of plasmacytoid dendritic cells (pDCs) (9) or associated with the expression of CXCR4 (83). Here, CXCR4 is linked to infection.