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Volume 16, Number 10, Issue of May 15, 1996 pp. 3139-3153
Copyright ©1996 Society for Neuroscience

Study of Receptor-Mediated Neurotoxins Released by HIV-1-Infected Mononuclear Phagocytes Found in Human Brain

Received Nov. 20, 1995; revised Feb. 14, 1996; accepted Feb. 20, 1996.

Dana Giulian1, Jiahan Yu1, Xia Li1, Donald Tom1, Jun Li1, Elaine Wendt1, Shen-Nan Lin2, Robert Schwarcz3, and Christine Noonan4,

1 Department of Neurology, Center for AIDS Research, Baylor College of Medicine, Houston, Texas 77030, 2 Analytical Chemistry Center, University of Texas-Houston Medical School, Houston, Texas 77030, 3 Maryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore, Maryland 21228, and 4 Division of Molecular Virology, Center for AIDS Research, Baylor College of Medicine, Houston, Texas 77030

Although there is growing evidence that neurotoxic molecules produced by HIV-1-infected mononuclear phagocytes damage neurons, the precise mechanisms of neuronal attack remain uncertain. One class of cytotoxin involves neuronal injury mediated via the NMDA receptor. We examined blood monocytes and brain mononuclear cells isolated at autopsy from HIV-1-infected individuals for the ability to release NMDA-like neuron-killing factors. We found that a neurotoxic amine, NTox, was produced by blood monocytes and by brain mononuclear phagocytes infected with retrovirus. In vivo injections of minute quantities of NTox produced selective damage to hippocampal pyramidal neurons. NTox can be extracted directly from brain tissues infected with HIV-1 and showed structural features similar to wasp and spider venoms. In contrast to NTox, HIV-1 infection did not increase the release of the NMDA excitotoxin quinolinic acid (QUIN) from mononuclear cells. Although we found modest elevations of QUIN in the CSF of HIV-1-infected individuals, the increases were likely attributable to entry through damaged blood-brain barrier. Taken together, our data pinpoint NTox, rather than QUIN, as a major NMDA receptor-directed toxin associated with neuro-AIDS.

Key words: AIDS; neurotoxin; gp120; microglia; macrophage; brain; dementia; HIV-1; NMDA; quinolinic acid




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