Biomedical Frontiers: Winter 1994, Vol.1, No.2
HIV may Use Novel Mechanism to Kill Neurons

Some of the neurological symptoms in HIV-infected patients can be attributed to immunodeficiency and opportunistic infections. But the causes for dementia, cognitive changes, and sensory neuropathy are still unknown.

Now results from in vitro studies by Dr. Norman Latov, associate professor of neurology, show that sensory neuropathy, or sensory loss and pain, may come about from HIV-1 binding to neurons and activating complement, causing neuronal lysis. (Immunological Investigations, in press.)

Dr. Latov and his team found that gp120, the viral surface glycoprotein from HIV-1, binds to the surface of cultured rat and human sensory neurons and activates complement, which lyses the neuronal cells. Neither gp120, complement, nor gp120 and deactivated complement kill neurons. Fibroblasts were unaffected by gp120 and complement.

gp120 does not use the CD4 receptor to bind to the neurons. Dr. Latov is attempting to isolate the receptor on the surface of neurons used by HIV with the hope of finding agents that inhibit its binding. Related research examines the role of HIV-infected macrophages in neuronal death. Since viral proteins are expressed on the surface of infected macrophages, cellular interactions between macrophages and neurons also may contribute to neuronal demise.

Approximately 50 percent of all patients with AIDS have cognitive changes. Between 20 percent and 50 percent have neuropathies independent of opportunistic infections. Both complications increase in incidence as the disease progresses.