Intraventricular injection of human immunodeficiency virus type 1 (HIV-1) tat protein causes inflammation, gliosis, apoptosis, and ventricular enlargement.
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| 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.
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| Authors | M Jones, K Olafson, M R Del Bigio, J Peeling, A Nath |
| Journal | Journal of neuropathology and experimental neurology (J Neuropathol Exp Neurol) Vol. 57 Issue 6 Pg. 563-70 (Jun 1998) ISSN: 0022-3069 [Print] England |
| PMID | 9630236 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
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