COMPLEMENT-DEPENDENT CYTOTOXICITY OF SENSORY GANGLION NEURONS MEDIATED BY THE GP120 GLYCOPROTEIN OF HIV-1

Patients infected with HIV-1 frequently have a sensory neuropathy, but the cause is unknown. We found that the gp120 glycoprotein of HIV-1 b ound to the surface of cultured rat dorsal root ganglia (DRG) neurons, and activated the complement cascade to lyse the neuronal cells. Cyto toxicity was measured by a Cr-51-release assay, and deposits of the C5 b-9 complement complex were detected on the affected cells. As control s, gp120 or complement alone, or rgpl20 plus deactivated complement, d id not damage the neuronal cells, and fibroblasts were unaffected. The gp120 glycoprotein can thereby damage DRG neurons by complement depen dent mechanisms. This interaction may contribute to the development of the sensory neuropathy in AIDS.