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HIV-related neurotoxicity.

¹Department of Neurology, Children's Hospital, Beth Israel Hospital, Brigham.

Brain Pathology (Zurich, Switzerland)

|April 1, 1991

Summary

HIV-1 envelope glycoprotein gp120 and other factors from infected cells cause neuronal injury in AIDS. Blocking calcium channels or NMDA receptors can protect neurons from this damage.

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Area of Science:

Neuroscience
Immunology
Virology

Background:

Acquired Immunodeficiency Syndrome (AIDS) central nervous system (CNS) pathology was initially characterized by white matter lesions.
Emerging evidence indicates significant neuronal loss also occurs in the CNS during AIDS.

Purpose of the Study:

To review evidence for human immunodeficiency virus (HIV)-related toxic factors contributing to neuronal injury.
To explore the role of HIV-1 envelope glycoprotein gp120 and macrophage-derived factors in neurotoxicity.

Main Methods:

Review of existing literature on HIV neurotoxicity.
Analysis of in vitro studies using rodent, chick, and human neurons exposed to gp120 or factors from HIV-infected macrophages/microglia.
Investigation of neuroprotective mechanisms involving calcium channel and glutamate receptor antagonists.

Main Results:

HIV-1 envelope glycoprotein gp120 induces intracellular calcium increase and delayed neurotoxicity in rodent neurons.
HIV-infected macrophages/microglia release undefined factors that cause neuronal death in vitro.
gp120-induced neurotoxicity is mitigated by L-type calcium channel blockers and N-methyl-D-aspartate (NMDA) receptor antagonists.
Glutamate appears to be a necessary synergistic factor in gp120-mediated neuronal injury.

Conclusions:

HIV-1 gp120 and factors released by infected immune cells contribute to neuronal loss in the CNS during AIDS.
Targeting calcium channels and NMDA receptors shows potential for preventing HIV-related neurotoxicity.
Further research is needed to elucidate the exact nature of macrophage-derived toxic factors and their relationship to gp120.

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