HIV-1 neuropathogenesis: Glial mechanisms revealed through substance abuse

Kurt F. Hauser, Nazira El-Hage, Anne Stiene-Martin, William F. Maragos, Avindra Nath, Yuri Persidsky, David J. Volsky, Pamela E. Knapp

Research output: Contribution to journalReview articlepeer-review

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 languageEnglish (US)
Pages (from-to)567-586
Number of pages20
JournalJournal of Neurochemistry
Volume100
Issue number3
DOIs
StatePublished - Feb 2007

Keywords

  • AIDS
  • Alcohol
  • Cocaine
  • HIV encephalopathy
  • Methamphetamine
  • Neuroimmunology
  • Opiates

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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