Modulation of astrocyte proliferation by HIV-1: Differential effects in productively infected, uninfected, and Nef-expressing cells
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.
Keywords: Cell cycle arrest, Human, Ki-67, BrdU, Vpr
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PII: S0165-5728(06)00193-7
doi:10.1016/j.jneuroim.2006.05.020
© 2006 Elsevier B.V. All rights reserved.
