Cortical consequences of HIV-1 Tat exposure in rats are enhanced by chronic cocaine.

Curr HIV Res

Department of Pharmacology, Rush University Medical Center, 1735 W. Harrison Street, Cohn Research Building, Rm. 463, Chicago, IL 60612, USA.

Published: December 2015

AI Article Synopsis

  • The lifespan of HIV-positive individuals has improved, but complications related to the central nervous system (CNS) remain significant issues.
  • HIV does not directly infect brain cells (neurons), but its proteins, especially Tat from infected glial cells, can have harmful effects on the brain.
  • Cocaine abuse among HIV-infected individuals worsens neurological problems, and this review examines the brain areas and mechanisms affected by both chronic cocaine use and HIV proteins.

Article Abstract

The life span of individuals that are sero-positive for human immunodeficiency virus (HIV) has greatly improved; however, complications involving the central nervous system (CNS) remain a concern. While HIV does not directly infect neurons, the proteins produced by the virus, including HIV transactivator of transcription (Tat), are released from infected glia; these proteins can be neurotoxic. This neurotoxicity is thought to mediate the pathology underlying HIVassociated neurological impairments. Cocaine abuse is common among HIV infected individuals, and this abuse augments HIV-associated neurological deficits. The brain regions and pathophysiological mechanisms that are dysregulated by both chronic cocaine and Tat are the focus of the current review.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896147PMC
http://dx.doi.org/10.2174/0929867322666150311164504DOI Listing

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