Feline immunodeficiency virus envelope protein (FIVgp120) causes electrophysiological alterations in rats

Close to 20% of the patients infected with the AIDS virus develops neurolog ical deficit; eventhough HIV does not invade neurons. Consistently with the neurological deficit, HIV+ subjects show abnormalities in brainstem audito ry and visual evoked potentials (BSAEP and VEP) and in sleep patterns. The HIV-derived glycoprotein 120 has been postulated as a neurotoxic; therefore , it may be playing a crucial role in the generation of BSAEP and VEP, as w ell as in sleep disturbances. To study the role of the virus-derived protei ns on the development of these electrophysiological signals' alterations, w e have used the feline immunodeficiency virus (FIV)-derived gp120 and evalu ated the changes in these electrophysiological signals. We employed 15 adul t male Sprague-Dawley rats (250-350 g), chronically implanted for evoked po tential and sleep recordings. Results showed that the i.c.v. administration of FIVgp120 (5 ng/10 mu l) produces changes in the latency of both cortica l auditory evoked potentials (CAEPs) and VEPs and a decrease in both REM sl eep and SWS. These data support the notion that FIVgp120 is neurotoxic to t he central nervous system of cats and rats and that this protein suffices t o cause electrophysiological alterations. In addition, it suggests that a s imilar effect may be occurring in humans as a result of HIVgp120's neurotox ic effects. (C) 1999 Elsevier Science B.V. All rights reserved.