In the event that this balance is disrupted, via the induction of an excessive inflammatory BMVEC phenotype by platelet-derived sCD40L within the plasma of HIV-infected individuals [17,44], it is plausible that sCD40L largely contributes to the increased permeability of the BBB seen during HAND, thereby increasing monocyte traffic at the BBB and invasion of the CNS by pro-inflammatory cells [26]. Here, CD40LG is linked to HIV-associated neurocognitive disorder.