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HIV-1 gp120 and morphine induced oxidative stress: role in cell cycle regulation

Thangavel Samikkannu1, Deepa Ranjith1, Kurapati V K Rao1

  • 1Department of Immunology, Institute of NeuroImmune Pharmacology, College of Medicine, Florida International University , Miami, FL, USA.

Frontiers in Microbiology
|July 10, 2015
PubMed

Insights

Morphine and HIV-1 infection increase oxidative stress, altering cell cycle proteins like CDK-1/CDC-2, cyclin B, and CDC-25C. This imbalance in human microglial cells suggests a mechanism for accelerated HIV progression and neurodegeneration.

Area of Science:

  • Neuroscience
  • Virology
  • Toxicology

Background:

  • HIV infection and illicit drug use, particularly morphine, are known to cause oxidative stress.
  • Oxidative stress is linked to increased viral replication, disease progression, impaired cell cycle regulation, and neurodegeneration.
  • Morphine's acceleration of HIV progression is mediated by reactive oxygen species (ROS), but its precise role in oxidative stress and cell cycle regulation remains unclear.

Purpose of the Study:

  • To elucidate the mechanism by which morphine and HIV-1 gp120 co-infection induce oxidative stress.
  • To investigate the impact of this oxidative stress on antioxidant enzymes: glutathione synthases (GSS), super oxide dismutase (SOD), and glutathione peroxidase (GPx).
  • To determine how these changes affect cell cycle regulatory proteins (CDK-1/CDC-2, cyclin B, CDC-25C) and influence neuronal dysfunction.

Main Methods:

  • Utilized a human microglial cell line exposed to HIV-1 gp120 and/or morphine.
  • Assessed the expression and activity of GSS, SOD, and GPx to evaluate oxidative stress.
  • Measured the levels of cell cycle proteins CDK-1/CDC-2, cyclin B, and CDC-25C.

Main Results:

  • Co-exposure to HIV-1 gp120 and morphine resulted in significant redox imbalance.
  • Glutathione synthases (GSS) and glutathione peroxidase (GPx) were inhibited, while super oxide dismutase (SOD) was increased.
  • CDK-1/CDC-2 expression was inhibited, whereas cyclin B and CDC-25C were significantly upregulated in the co-infected group compared to single-agent treatment.

Conclusions:

  • HIV-1 gp120 and morphine co-infection significantly elevates oxidative stress in human microglial cells.
  • This oxidative stress profoundly affects the cell cycle machinery, leading to the inhibition of CDK-1/CDC-2 and upregulation of cyclin B and CDC-25C.
  • These findings suggest a potential mechanism for accelerated HIV disease progression and neurodegeneration in individuals using morphine concurrently with HIV infection.
Keywords:
HIV-1 gp120cell cycle and microgliamorphineoxidative stress

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