Encephalopathy represents a common and serious manifestation of HIV-1 infec
tion in children, but its pathogenesis is unclear. We demonstrated that gp1
20 activated human brain microvascular endothelial cells (HBMEC) derived fr
om children in up-regulating ICAM-1 and VCAM-1 expression, IL-6 secretion a
nd increased monocyte transmigration across monolayers. Another novel obser
vation was our demonstration of CD4 in isolated HBR-IEC and on microvessels
of children's brain cryosections. Gp120-induced monocyte migration was inh
ibited by anti-gp120 and anti CD4 antibodies. This is the first demonstrati
on that gp120 activates HBMEC via CD4, which may contribute to the developm
ent of HIV-1 encephalopathy in children.