Intraventricular injection of human immunodeficiency virus type 1 (HIV- 1) Tat protein causes inflammation, gliosis, apoptosis, and ventricular enlargement

Melina Jones, Kendiss Olafson, Marc R. Del Bigio, James Peeling, Avindra Nath

Research output: Contribution to journalArticle

Abstract

To determine the role of the Tat protein of the human immunodeficiency virus type 1 (HIV-1) in the pathogenesis of HIV-1 associated dementia, recombinant Tat was injected intraventricularly as a single or repeated dose into male Sprague-Dawley rats. Histopathological evaluation showed an initial infiltration of neutrophils one day after Tat injection, followed by macrophages and lymphocytes by 7 days. Tat-injected brains also exhibited astrocytosis, apoptotic cells, and ventricular enlargement 7 days following the last injection. Nuclear magnetic resonance spectroscopic analysis of tissue extracts of hippocampi from Tat-injected rats showed a decrease in the glutamate/g aminobutyric acid ratio. We conclude that the transient extracellular exposure of the central nervous system to Tat protein of HIV can cause a cascade of events leading to the influx of inflammatory cells, glial cell activation, and neurotoxicity.

Original languageEnglish (US)
Pages (from-to)563-570
Number of pages8
JournalJournal of neuropathology and experimental neurology
Volume57
Issue number6
DOIs
StatePublished - Jun 1998

Keywords

  • AIDS
  • Apoptosis
  • Brain
  • HIV-1
  • Inflammation
  • NMR
  • Tat

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

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