“…HIV infection has been implicated as the etiological factor in many published cases of PRES [8,9,11,13]. HIV virus has been shown to induce endothelial cell apoptosis, tight junction disruption, oxidative stress, and the expression of pro-inflammatory cytokines and adhesion molecules which stimulate endothelial cell inflammation, all of which culminates in BBB dysfunction [11,16,17]. Most reported cases of PRES occurred in patients with low CD4 counts (range 16–284 cells/ μ l) [9,13,18–21], however, HIV-induced pathology has not been shown to be related to viral load [22].…”