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A Randomized, Placebo-Controlled, Pilot Clinical Trial of Dipyridamole to Decrease Human Immunodeficiency

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The Journal of Infectious Diseases
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Dipyridamole therapy in people with HIV-1 increased extracellular adenosine, reducing T-cell immune activation. This suggests a potential strategy for managing chronic inflammation in HIV patients on antiretroviral therapy.

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Area of Science:

  • Immunology
  • Pharmacology
  • Virology

Background:

  • Adenosine is a key immunoregulatory nucleoside that limits tissue damage during inflammation.
  • Chronic inflammation is a hallmark of human immunodeficiency virus (HIV) type 1 infection.
  • Dipyridamole inhibits adenosine uptake, potentially increasing extracellular adenosine levels to mitigate inflammation.

Purpose of the Study:

  • To investigate the effect of dipyridamole on extracellular adenosine levels and T-cell activation in virally suppressed HIV-1 infected individuals.
  • To assess dipyridamole's impact on systemic inflammation markers.

Main Methods:

  • A randomized, double-blind, placebo-controlled trial involving virally suppressed participants on antiretroviral therapy.
  • Participants received dipyridamole (100 mg 4 times daily) or placebo for 12 weeks, followed by open-label dipyridamole for 12 weeks.
  • End points included changes in inflammatory markers (soluble CD163, CD14, IL-6) and T-cell activation (HLA-DR+CD38+).

Main Results:

  • No significant changes were observed in most systemic inflammatory markers, though a trend towards decreased soluble CD163 was noted.
  • A modest, though not statistically significant in pooled analysis, decrease in CD8+ T-cell activation was observed with dipyridamole.
  • Dipyridamole significantly reduced CD4+ T-cell activation in pooled analyses.

Conclusions:

  • Dipyridamole effectively increased extracellular adenosine levels in individuals with HIV-1.
  • The drug demonstrated a significant decrease in T-cell activation, suggesting a role in managing immune dysregulation in HIV.
  • These findings support dipyridamole as a potential therapeutic agent for dampening chronic inflammation in HIV-1 infection.