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Alcohol and HIV decrease proteasome and immunoproteasome function in macrophages: implications for impaired immune

James Haorah1, David Heilman, Casey Diekmann

  • 1Liver Study Unit, The Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, NE 68198-5215, USA.

Cellular Immunology
|October 12, 2004
PubMed
Summary
This summary is machine-generated.

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HIV-1 infection and alcohol impair proteasome (PR) and immunoproteasome (IPR) function, crucial for immune response. Antioxidants may restore proteasome activity suppressed by alcohol in HIV-1 infected cells.

Area of Science:

  • Immunology
  • Cellular Biology
  • Virology

Background:

  • Proteasomes (PR) and immunoproteasomes (IPR) are vital for protein degradation and antigen presentation.
  • HIV-1 infection and alcohol abuse negatively impact these immune functions.
  • Understanding these interactions is critical for managing HIV-1 progression.

Purpose of the Study:

  • To investigate the combined effects of HIV-1 infection and ethanol (EtOH) on proteasome and immunoproteasome activity.
  • To explore the role of reactive oxygen species (ROS) in mediating these effects.
  • To assess potential therapeutic interventions like antioxidants.

Main Methods:

  • Human monocyte-derived macrophages (MDM) were infected with HIV-1 and treated with ethanol (EtOH).
  • Proteasome (PR) and immunoproteasome (IPR) activities and contents were measured.

Related Experiment Videos

  • CYP2E1 activity, ethanol metabolizing enzyme, and reactive oxygen species (ROS) were assessed.
  • Interferon-gamma (IFN-γ) stimulation and antioxidant treatment were employed.

    • Main Results:

    • HIV-1 infection progressively reduced PR activity and PR/IPR content in MDM.
    • Ethanol inhibited IFN-γ-induced PR and IPR activity.
    • Ethanol attenuated PR activity in HIV-1 infected MDM, paradoxically suppressing viral replication.
    • Elevated ROS levels correlated with decreased PR activity, which was reversed by antioxidants.

    Conclusions:

    • HIV-1 infection and ethanol synergistically impair proteasome and immunoproteasome function.
    • Ethanol-induced ROS contribute to proteasome inhibition in HIV-1 infected macrophages.
    • These combined effects may compromise immune function and influence HIV-1 disease progression.
    • Antioxidants show potential in mitigating alcohol-induced proteasome dysfunction in HIV-1 infection.