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Related Experiment Videos

Human immunodeficiency virus causes mononuclear phagocyte dysfunction.

G C Baldwin1, J Fleischmann, Y Chung

  • 1Division of Hematology-Oncology, UCLA School of Medicine 90024.

Proceedings of the National Academy of Sciences of the United States of America
|May 1, 1990
PubMed
Summary

Human immunodeficiency virus (HIV) infection impairs macrophage function, reducing their ability to kill pathogens and tumor cells. Early treatment with azidothymidine (AZT) can restore macrophage function by decreasing viral load.

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Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Mononuclear phagocyte system dysfunction is observed in acquired immunodeficiency syndrome (AIDS) patients, potentially due to T-cell loss.
  • The direct impact of human immunodeficiency virus (HIV) on macrophage function remains unclear.

Purpose of the Study:

  • To investigate the direct effects of HIV infection on human macrophage functions, specifically their extra- and intracellular killing capabilities.

Main Methods:

  • Normal human macrophages were infected in vitro with a monocytotropic strain of HIV.
  • Assays were performed to quantify the antibody-dependent cell-mediated cytotoxicity (ADCC) and intracellular killing of Candida pseudotropicalis.

Main Results:

  • HIV-infected macrophages exhibited significantly reduced efficacy in ADCC against leukemic targets and intracellular killing of C. pseudotropicalis compared to control cells.

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  • These functional defects correlated with active virus production and were not improved by granulocyte-macrophage colony-stimulating factor.
  • Treatment with 3'-azido-3'-deoxythymidine (AZT) post-infection decreased viral production and prevented the development of impaired intracellular killing.

    • Conclusions:

    • HIV directly impairs critical macrophage functions, impacting host defense mechanisms.
    • Early antiviral therapy, such as AZT, may preserve macrophage function by controlling viral replication.