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HIV-1 Vpr induces defects in mitosis, cytokinesis, nuclear structure, and centrosomes

Fred Chang1, Fabio Re, Sarah Sebastian

  • 1Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.

Molecular Biology of the Cell
|February 10, 2004
PubMed

Insights

The Human Immunodeficiency Virus type 1 (HIV-1) Vpr protein disrupts cell division by affecting mitotic spindle assembly and function. This leads to defects in cell division and centrosome abnormalities, potentially explaining HIV-1 associated pathologies.

Area of Science:

  • Cell Biology
  • Virology
  • Molecular Biology

Background:

  • The Human Immunodeficiency Virus type 1 (HIV-1) accessory protein Vpr is known to interfere with cell cycle progression.
  • Previous research indicated Vpr's role in inhibiting G2/M cell cycle arrest in both human and yeast cells.

Purpose of the Study:

  • To investigate the effects of HIV-1 Vpr expression on mitotic spindle assembly and function.
  • To explore the impact of Vpr on cell division processes like mitosis and cytokinesis in model organisms and human cells.

Main Methods:

  • Induction of vpr gene expression in fission yeast (Schizosaccharomyces pombe).
  • Microscopic analysis of spindle pole body proteins (sad1p, plo1p), nuclear envelope, actin ring, and cytokinesis.
  • Observation of similar cellular defects in human cells expressing Vpr.

Main Results:

  • Vpr expression in fission yeast caused defects in mitotic spindle assembly and function.
  • Spindle pole body proteins sad1p and plo1p were delocalized, indicating perturbed spindle pole body integrity.
  • Nuclear envelope, contractile actin ring formation, and cytokinesis were disrupted in yeast; similar defects were observed in human cells, including aberrant mitotic spindles, multiple centrosomes, and multinucleation.

Conclusions:

  • HIV-1 Vpr significantly perturbs mitosis and cytokinesis by disrupting spindle pole body integrity and centrosome function.
  • These Vpr-induced cellular defects may contribute to the pathology observed in HIV-1 infection.
  • The study highlights Vpr's role beyond cell cycle arrest, impacting fundamental cell division processes.

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