During the last few years several studies have been undertaken to char
acterise the role of gp120, the HIV-1 envelope glycoprotein, in the ph
atogenesis of neurological defects associated with AIDS. However, neur
ons did not appear to be the main target of the virus, since the wides
pread neuronal damage is not associated with a productive viral infect
ion in neurons. The current opinion supports the hypothesis that an in
direct mechanism exists to explain the neuronal cell death which occur
s in patients infected by HIV-1. In particular, several reports sugges
t that gp120 may be the main candidate as mediator of the neurological
deficits during HIV-1 infection and demonstrate that this molecule af
fects neuronal survival through a direct interaction with non-neuronal
cell types such as monocytes, macrophages/microglia and astrocytes. (
C) 1998 Elsevier Science Inc.