Modulation of astrocyte proliferation by HIV-1: Differential effects in productively infected, uninfected, and Nef-expressing cells

Melissa A. Cosenza-Nashat, Qiusheng Si, Meng Liang Zhao, Sunhee C. Lee

Research output: Contribution to journalArticle

11 Scopus citations

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 languageEnglish (US)
Pages (from-to)87-99
Number of pages13
JournalJournal of Neuroimmunology
Volume178
Issue number1-2
DOIs
StatePublished - Sep 1 2006

Keywords

  • BrdU
  • Cell cycle arrest
  • Human
  • Ki-67
  • Vpr

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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