Abstract
Although quiescent in normal brain, reactive astrocytes can proliferate in various disorders. We examined the impact of HIV-1 on astrocyte proliferation in cultures exposed to VSVg env-pseudotyped HIV-1 which yields high levels of infection. HIV-1, while increasing the proliferation of uninfected (p24-) astrocytes, strongly inhibited proliferation of productively infected (p24+) cells. The cell cycle arrest was G1/S rather than G2/M, a type commonly attributed to Vpr. No clear role of Vpr or Nef could be identified. Adenovirus-mediated expression of Nef (a model of "restricted" infection) induced M-phase arrest of astrocytes. We speculate that HIV-1 is a significant modulator of astrocyte proliferation in vivo.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 87-99 |
| Number of pages | 13 |
| Journal | Journal of Neuroimmunology |
| Volume | 178 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Sep 2006 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- BrdU
- Cell cycle arrest
- Human
- Ki-67
- Vpr
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology
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