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Updated: Nov 20, 2025

Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques
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Demystifying Cell Cycle Arrest by HIV-1 Vif.

Daniel J Salamango1, Reuben S Harris2

  • 1Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA; Institute for Molecular Virology, University of Minnesota, Minneapolis, MN 55455, USA.

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|January 22, 2021
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The human immunodeficiency virus type 1 (HIV-1) Vif protein, beyond degrading APOBEC3, triggers significant cell cycle arrest. This viral protein

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G2/M cell cycle arrestHIV-1PPP2R5Vifhost–pathogen interaction

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Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • The human immunodeficiency virus type 1 (HIV-1) Vif protein is primarily known for its role in degrading APOBEC3 proteins.
  • A newly identified function of HIV-1 Vif is its ability to induce potent cell cycle arrest in host cells.

Purpose of the Study:

  • To review recent advancements in understanding the mechanism of HIV-1 Vif-induced cell cycle arrest.
  • To explore the broader implications of this Vif activity beyond host cell cycle subversion.

Main Methods:

  • Review of existing scientific literature on HIV-1 Vif function and host cell cycle regulation.
  • Analysis of recent experimental findings related to Vif's interaction with cellular machinery.

Main Results:

  • HIV-1 Vif induces cell cycle arrest through a distinct, newly defined mechanism.
  • This mechanism appears to have functions extending beyond the mere manipulation of the host cell cycle.

Conclusions:

  • The role of HIV-1 Vif in cell cycle regulation is more complex than previously understood.
  • Further research is warranted to fully elucidate the scope and impact of Vif's cell cycle-related activities.