HIV-1 Vpr and G2 cell cycle arrest
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Updated: Jun 2, 2026

Analysis of Cell Cycle Position in Mammalian Cells
Published on: January 21, 2012
Masako Nomaguchi1, Akio Adachi
1Department of Microbiology, Institute of Health Biosciences, The University of Tokushima Graduate School, Kuramoto, Tokushima, Japan.
Abstract:
Evaluation of: Belzile J-P, Abrahamyan LG, Gerard FCA et al.: Formation of mobile chromatin-associated nuclear foci containing HIV-1 Vpr and VPRBP is critical for the induction of G2 cell cycle arrest. PLoS Pathog. 6(9), E1001080 (2010). All primate immunodeficiency viruses encode a unique set of accessory proteins to optimize their replication in hosts. In general, these proteins appear to be multifunctional for virus replication. Viral protein R (Vpr), one of the accessory proteins, has also been reported to exhibit distinct activities, but its exact role in the viral life cycle is still unclear and controversial. However, of particular note, Vpr-mediated G2 cell cycle arrest is conserved among primate immunodeficiency viruses. Belzile et al. have characterized and analyzed in detail the punctuate structures on the DNA of host cells formed by HIV-1 Vpr (Vpr nuclear foci). They demonstrate, mainly by confocal immunofluorescence analysis, that highly mobile chromatin-associated Vpr nuclear foci are critical for induction of the G2 cell cycle arrest.
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