Since several studies have shown that cerebrovascular endothelial cells are strong gatekeepers and regulators of HIV infection, not likely permissive to infection, yet affected be HIV peptides such as Tat, Nef and gp120 and by chronic inflammation [75, 76], we deem that the damage to the BBB in the model is indirect, perhaps in part by residual viral peptides, but most likely due to the increased TNFa (used as a positive control for damage), along with other vasoactive cytokines. This evidence concerns the gene TNF and infection.