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gp120-mediated alterations in astrocyte ion transport
D J Benos1, B H Hahn, G M Shaw
1Department of Physiology and Biophysics, University of Alabama at Birmingham 35294.
Advances in Neuroimmunology
|January 1, 1994
Summary
The human immunodeficiency virus (HIV) envelope glycoprotein gp120 may cause acquired immunodeficiency syndrome (AIDS) dementia complex by altering astrocyte function. This disruption in ion and solute transport could lead to neuronal injury.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- The exact cause of acquired immunodeficiency syndrome (AIDS) dementia complex (ADC) remains unclear.
- Existing research suggests that HIV-1 infection compromises neuronal and astrocyte function through viral components or factors from infected macrophages/microglia.
Purpose of the Study:
- To investigate the impact of the major HIV envelope glycoprotein gp120 on primary cultured rat astrocytes.
- To determine if gp120 exposure alters astrocyte ion and solute transport mechanisms.
Main Methods:
- Primary rat astrocytes were cultured in vitro.
- Astrocytes were exposed to the HIV envelope glycoprotein gp120.
- Ion and solute transport functions of the astrocytes were subsequently analyzed.
Main Results:
- Exposure of primary cultured rat astrocytes to gp120 resulted in significant alterations in ion transport.
- Solute transport mechanisms in astrocytes were also affected by gp120 exposure.
- These transport alterations suggest a potential mechanism for neuronal damage in ADC.
Conclusions:
- The HIV envelope glycoprotein gp120 can directly impair astrocyte function.
- Alterations in astrocyte ion and solute transport induced by gp120 may contribute to the pathogenesis of AIDS dementia complex.
- Further research is warranted to fully elucidate the role of gp120 in HIV-associated neurotoxicity.