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

doi:10.1016/j.jneuroim.2006.05.020

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

Pathology

Research output: Contribution to journal › Article › peer-review

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 language	English (US)
Pages (from-to)	87-99
Number of pages	13
Journal	Journal of Neuroimmunology
Volume	178
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2006.05.020
State	Published - Sep 2006

Keywords

BrdU
Cell cycle arrest
Human
Ki-67
Vpr

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.jneuroim.2006.05.020

Cite this

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title = "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 = "BrdU, Cell cycle arrest, Human, Ki-67, Vpr",

author = "Cosenza-Nashat, {Melissa A.} and Qiusheng Si and Zhao, {Meng Liang} and Lee, {Sunhee C.}",

note = "Funding Information: We thank the Einstein Fetal Tissue Repository for the tissue and Wa Shen for the astrocyte cultures. Several reagents used in this study were acquired from the NIH AIDS Research and Reference Reagent Program. We appreciate the assistance of the laboratories of Drs. Richard Kitisis, Peter Davies and Liang Zhu at the Albert Einstein College of Medicine for the helpful discussion and reagents. Hannah Suh and Joseph Choi assisted with the Western blot analysis while this study was progressing, and their efforts are greatly appreciated. This study was supported by the MH55477 and the Einstein CFAR AI051519. MCN and QS were in part supported by the Neuropathology Training Grant NS07098. This report is a component of a thesis submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate Division of Medical Sciences, Albert Einstein College of Medicine. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.",

year = "2006",

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language = "English (US)",

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AU - Zhao, Meng Liang

AU - Lee, Sunhee C.

N1 - Funding Information: We thank the Einstein Fetal Tissue Repository for the tissue and Wa Shen for the astrocyte cultures. Several reagents used in this study were acquired from the NIH AIDS Research and Reference Reagent Program. We appreciate the assistance of the laboratories of Drs. Richard Kitisis, Peter Davies and Liang Zhu at the Albert Einstein College of Medicine for the helpful discussion and reagents. Hannah Suh and Joseph Choi assisted with the Western blot analysis while this study was progressing, and their efforts are greatly appreciated. This study was supported by the MH55477 and the Einstein CFAR AI051519. MCN and QS were in part supported by the Neuropathology Training Grant NS07098. This report is a component of a thesis submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate Division of Medical Sciences, Albert Einstein College of Medicine. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.

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N2 - 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.

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

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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