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.
authors.affiliation: Borough of Manhattan Community College, City University of New York, Department of Science, New York, NY 10007, USA.
authors.forename: Melissa A
authors.initials: MA
authors.lastname: Cosenza-Nashat
authors.forename: Qiusheng
authors.initials: Q
authors.lastname: Si
authors.forename: Meng-Liang
authors.initials: ML
authors.lastname: Zhao
authors.forename: Sunhee C
authors.initials: SC
authors.lastname: Lee
mesh_terms: D001253:Astrocytes / Q000166:cytology / Q000378:metabolism / Q000821:virology*; D015153:Blotting, Western; D002453:Cell Cycle / Q000502:physiology; D049109:Cell Proliferation; D002478:Cells, Cultured; D015658:HIV Infections / Q000503:physiopathology*; D015497:HIV-1 / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D015728:Receptors, HIV / Q000096:biosynthesis*
chemical_list: C110852:Nef receptor; D015728:Receptors, HIV