HIV-1 neuropathogenesis: Glial mechanisms revealed through substance abuse Article

cited authors

  • Hauser, KF; El-Hage, N; Stiene-Martin, A; Maragos, WF; Nath, A; Persidsky, Y; Volsky, DJ; Knapp, PE

fiu authors

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. © 2007 The Authors.

publication date

  • February 1, 2007

Digital Object Identifier (DOI)

start page

  • 567

end page

  • 586

volume

  • 100

issue

  • 3