Glia are the predominant brain cells infected by the lentiviruses huma
n immunodeficiency virus (HIV) and feline immunodeficiency virus (FIV)
. The importance of astrocytes in maintenance of central nervous syste
m homeostasis suggests that astrocytes are likely to play a strategic
role in the progression of neurological disease in lentiviral-infected
patients. In consideration of this postulate, the ability of FIV to c
ause injury by infection of cultured feline astroglia was examined via
vital fluorescence assays. Intracellular Ca2+ homeostasis, plasma mem
brane permeability and fluidity, and cytosolic glutathione (GSH) level
s were evaluated. Although basal intracellular Ca2+ was not significan
tly different between groups, FIV-infected astroglia displayed both a
significant delay in development of peak Ca2+ levels following ionopho
re application and a decrease in the amount of Ca2+ released from intr
acellular stores. Plasma membrane lipid mobility was increased in FIV-
infected cells within 24 h of infection. Glutathione levels were affec
ted in a dose dependent fashion. With a standard viral inoculum there
was a decrease in GSH which became significant after 8 days postinfect
ion With a high inoculum dose there was rapid loss of cell viability w
ith an increase in GSH in surviving cells. We have identified several
cellular processes altered in FN-infected astroglia and our findings s
uggest that FIV-infection of feline astroglia affects cellular membran
es, both structurally and functionally. (C) 1995 Wiley-Liss, Inc.