While in vivo exposure to Tat alone as an experimental model for HIV-1 neuropathogenesis clearly has its limitations, other murine models of HIV-1 infection of the CNS [22], [23], [58] are not compatible with the adoptive transfer methodologies required to dissect the relative contribution of peripheral leukocytes vs. microglia in HIV-1 induced neuroinflammation. This evidence concerns the gene TAT and HIV-1 infection.