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J. Virol., Oct 1995, 6304-6313, Vol 69, No. 10
JB Jowett, V Planelles, B Poon, NP Shah, ML Chen and IS Chen
Human immunodeficiency virus type 1 (HIV-1) infection causes profound
immunological defects in afflicted patients. Various mechanisms have been
proposed to account for the immune dysfunction in AIDS ultimately leading
to loss of CD4+ T cells, including HIV-1 envelope-mediated syncytium
formation, apoptosis, and cytokine modulation. Here we present results
which suggest a novel hypothesis for T-cell dysfunction. We show, using
HIV-1 bearing a novel cell surface reporter gene, that infected cells are
unable to progress normally through the cell cycle and became arrested in
the G2 + M phase. Furthermore, we identify the HIV-1 vpr gene product as
being both necessary and sufficient for eliciting this cell cycle arrest.
Cell cycle arrest induced by Vpr correlates with an increase in the
hyperphosphorylated (inactive) form of the cyclin-dependent
serine/threonine kinase CDC2, consistent with an arrest of cells at the
boundary of G2 and M.
Copyright © 1995, American Society for Microbiology
The human immunodeficiency virus type 1 vpr gene arrests infected T cells in the G2 + M phase of the cell cycle
Department of Microbiology & Immunology, UCLA School of Medicine 90095- 1678, USA.
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