Complement dependent cytotoxicity of sensory ganglion neurons mediated by the gp120 glycoprotein of HIV-1.

Overview

Patients infected with HIV-1 frequently have a sensory neuropathy, but the cause is unknown. We found that the gp120 glycoprotein of HIV-1 bound to the surface of cultured rat dorsal root ganglia (DRG) neurons, and activated the complement cascade to lyse the neuronal cells. Cytotoxicity was measured by a 51Cr-release assay, and deposits of the C5b-9 complement complex were detected on the affected cells. As controls, gp120 or complement alone, or rgp120 plus deactivated complement, did not damage the neuronal cells, and fibroblasts were unaffected. The gp120 glycoprotein can thereby damage DRG neurons by complement dependent mechanisms. This interaction may contribute to the development of the sensory neuropathy in AIDS.