Impaired inflammatory functions may be critical factors in the mechanisms by which HIV-1
enters the CNS. Evidence indicates that a viral gene product, the protein Tat, can markedly
contribute to these effects. In the present study we tested the hypothesis that Tat can
upregulate the expression of inflammatory cytokines and adhesion molecules and facilitate
the entry of monocytes into the brain. Expression of inflammatory mediators such as
monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), vascular cell …