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Related Experiment Videos

Human immunodeficiency virus type 1 Vpr alters bone marrow cell function.

J Kulkosky1, A Laptev, S Shetty

  • 1Dorrance H. Hamilton Laboratories, Center for Human Virology, Division of Infectious Diseases, Department of Medicine, Jefferson Medical College, Jefferson University, Philadelphia, PA, USA.

Blood
|March 9, 1999
PubMed
Summary

The human immunodeficiency virus type I (HIV-1) Vpr protein activates immune cells in bone marrow cultures. This Vpr protein promotes phagocytosis, potentially explaining HIV-1 infection and cytopenias in patients.

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Area of Science:

  • Virology
  • Immunology
  • Hematology

Background:

  • The Vpr protein of human immunodeficiency virus type I (HIV-1) is crucial for infecting mononuclear phagocytic cells.
  • These cells are prevalent in bone marrow, a site supporting hematopoiesis.
  • Previous research highlighted Vpr's role in HIV-1 pathogenesis.

Purpose of the Study:

  • To investigate the role of Vpr in activating mononuclear phagocytic cells within a hematopoietic microenvironment.
  • To determine if Vpr induces specific cellular responses like phagocytosis.
  • To explore the potential implications of Vpr-mediated activation in HIV-1 infection and associated cytopenias.

Main Methods:

  • Culturing murine and human bone marrow cells in vitro.
  • Transducing marrow cells with retroviral vectors expressing Vpr.

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  • Treating marrow cultures with purified Vpr protein.
  • Observing and quantifying cellular adhesion and phagocytosis.

    • Main Results:

    • Vpr expression in murine marrow cells triggered avid erythrophagocytosis.
    • Vpr treatment of human marrow cells promoted mononuclear phagocyte adhesion and engulfment.
    • Mutant Vpr proteins showed differential effects, confirming Vpr specificity.
    • Extracellular Vpr was identified as the effector molecule promoting cell adhesion and phagocytosis.

    Conclusions:

    • HIV-1 Vpr protein specifically activates mononuclear phagocytic cells within the hematopoietic microenvironment.
    • Vpr-induced phagocytosis in bone marrow may contribute to productive viral infection.
    • Accelerated phagocytosis by Vpr may explain the idiopathic cytopenias observed in HIV-1-infected individuals.