Modulation of astrocyte proliferation by HIV-1: differential effects in productively infected, uninfected, and Nef-expressing cells.
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.
Cosenza-Nashat
Melissa A
MA
Borough of Manhattan Community College, City University of New York, Department of Science, New York, NY 10007, USA.
Si
Qiusheng
Q
Zhao
Meng-Liang
ML
Lee
Sunhee C
SC
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*
C110852:Nef receptor; D015728:Receptors, HIV