Abstract
Neuronal dysfunction and degeneration are ultimately responsible for the neurocognitive impairment and dementia manifest in neuroAIDS. Despite overt neuronal pathology, HIV-1 does not directly infect neurons; rather, neuronal dysfunction or death is largely an indirect consequence of disrupted glial function and the cellular and viral toxins released by infected glia. A role for glia in HIV-1 neuropathogenesis is revealed in experimental and clinical studies examining substance abuse-HIV-1 interactions. Current evidence suggests that glia are direct targets of substance abuse and that glia contribute markedly to the accelerated neurodegeneration seen with substance abuse in HIV-1 infected individuals. Moreover, maladaptive neuroplastic responses to chronic drug abuse might create a latent susceptibility to CNS disorders such as HIV-1. In this review, we consider astroglial and microglial interactions and dysfunction in the pathogenesis of HIV-1 infection and examine how drug actions in glia contribute to neuroAIDS.
Original language | English (US) |
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Pages (from-to) | 567-586 |
Number of pages | 20 |
Journal | Journal of Neurochemistry |
Volume | 100 |
Issue number | 3 |
DOIs | |
State | Published - Feb 2007 |
Externally published | Yes |
Keywords
- AIDS
- Alcohol
- Cocaine
- HIV encephalopathy
- Methamphetamine
- Neuroimmunology
- Opiates
ASJC Scopus subject areas
- Biochemistry
- Cellular and Molecular Neuroscience