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Updated: May 20, 2026
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A Rat Model of EcoHIV Brain Infection
Published on: January 21, 2021
Human immunodeficiency virus type 1 alters brain-derived neurotrophic factor processing in neurons
Alessia Bachis1, Valeriya Avdoshina, Luigi Zecca
1Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057, USA.
Summary
Human immunodeficiency virus (HIV) protein gp120 alters brain-derived neurotrophic factor (BDNF) processing, leading to neurotoxicity. This gp120-induced imbalance in pro-BDNF and mature BDNF contributes to neuronal injury in HIV subjects.
Area of Science:
- Neuroscience
- Molecular Biology
- Virology
Background:
- Synaptic simplification and neuronal apoptosis in HIV-1 infection are not fully understood.
- The HIV protein gp120 mimics the neurotoxic effects of pro-brain-derived neurotrophic factor (proBDNF) via the p75 neurotrophin receptor.
Purpose of the Study:
- To investigate the hypothesis that HIV gp120 affects proBDNF release and processing.
- To elucidate the molecular mechanisms underlying HIV-induced neurotoxicity.
Main Methods:
- Primary rat neurons were treated with gp120 to assess proBDNF and mature BDNF levels.
- Levels of intracellular furin and extracellular tissue plasminogen were measured.
- Postmortem brain tissues from HIV-positive subjects with cognitive and motor impairments were analyzed.
Main Results:
- Gp120 exposure led to increased intracellular and extracellular proBDNF accumulation and decreased mature BDNF.
- An imbalance in the proBDNF/mature BDNF ratio was observed in HIV-positive subjects' brains.
- Gp120 reduced intracellular furin levels, suggesting impaired proBDNF processing.
Conclusions:
- HIV-induced neurotoxicity involves gp120-mediated alteration of BDNF processing, specifically by reducing furin levels.
- This disruption leads to an imbalance between antiapoptotic and proapoptotic neurotrophins, contributing to neuronal injury.
