Abstract
Macrophages and microglia are the predominant cells infected with HIV-1 in the brain, yet the effects of productive HIV infection on the fate of these cells are poorly understood. In this study, we tested the hypothesis that HIV-1 expression influences cell death in infected macrophages and microglial cells. We detected apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) in the cerebral white matter of control and HIV encephalitis (HIVE) brains, and quantitatively analysed apoptotic cells with respect to their location (vessel-associated vs. parenchymal), CD68 expression, and HIV-1 p24 expression. There were more vessel-associated, but not more parenchymal, TUNEL+ cells in HIVE cases as compared to controls. Vessel-associated TUNEL+ cells were primarily endothelial cells (von Willebrand factor+) or macrophages (CD68+). TUNEL+/CD68+ cells were present in both control and HIVE cases in similar frequencies (2.1 ± 0.7% vs. 1.9 ± 0.7% of total CD68+ populations, respectively). In HIVE, TUNEL+/p24+ cells were 0.4 ± 0.2% of the total p24+ cell population, which was lower than the frequency of TUNEL+/CD68+ cells (1.9 ± 0.7%) in the total CD68+ macrophage population. These results suggest that HIV-1-infected macrophages and microglia are resistant to apoptosis. and may contribute to the formation of a central nervous system viral reservoir.
Original language | English (US) |
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Pages (from-to) | 478-490 |
Number of pages | 13 |
Journal | Neuropathology and Applied Neurobiology |
Volume | 30 |
Issue number | 5 |
DOIs | |
State | Published - Oct 2004 |
Keywords
- AIDS
- Apoptosis
- HIV encephalitis
- Perivascul
- Productive infection
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Histology
- Neurology
- Clinical Neurology
- Physiology (medical)