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
StatePublished - Jun 1998
Externally publishedYes

Fingerprint

tat Gene Products
Intraventricular Injections
Gliosis
HIV-1
Human Immunodeficiency Virus tat Gene Products
Cell Enlargement
Apoptosis
Inflammation
Aminobutyrates
Injections
Tissue Extracts
Neutrophil Infiltration
Neuroglia
Sprague Dawley Rats
Dementia
Glutamic Acid
Hippocampus
Magnetic Resonance Spectroscopy
Central Nervous System
Macrophages

Keywords

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

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neuroscience(all)

Cite this

Intraventricular injection of human immunodeficiency virus type 1 (HIV- 1) Tat protein causes inflammation, gliosis, apoptosis, and ventricular enlargement. / Jones, Melina; Olafson, Kendiss; Del Bigio, Marc R.; Peeling, James; Nath, Avindra.

In: Journal of Neuropathology and Experimental Neurology, Vol. 57, No. 6, 06.1998, p. 563-570.

Research output: Contribution to journalArticle

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