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Shared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndrome

Nicholas T Funderburg1, David A Zidar, Carey Shive

  • 1Department of Medicine, Division of Infectious Diseases, Case Western Reserve University/University Hospitals of Cleveland, Cleveland, OH 44106, USA. NTF1@case.edu

Blood
|October 16, 2012
PubMed

Insights

HIV-1 infection alters monocyte subsets, increasing cardiovascular risk. Specific monocyte profiles in HIV-1 patients mirror those seen in acute coronary syndrome, suggesting shared inflammatory drivers.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Virology

Background:

  • The mechanisms linking human immunodeficiency virus type 1 (HIV-1) infection to increased cardiovascular risk are not fully understood.
  • Monocyte subpopulations play a crucial role in immune responses and inflammation, potentially contributing to atherosclerosis.

Purpose of the Study:

  • To investigate and compare the activation phenotypes of monocyte subpopulations in individuals with HIV-1 infection and those with acute coronary syndrome (ACS).
  • To identify common cellular profiles that may explain the elevated cardiovascular risk in HIV-1 infection.

Main Methods:

  • Flow cytometry was employed to analyze monocyte subpopulations (nonclassic and intermediate) and their activation markers (tissue factor, CD62P).
  • Whole blood samples from HIV-1 infected individuals and ACS patients were compared to healthy controls.
  • In vitro experiments exposed control blood to lipopolysaccharide (LPS) and HIV-1 to assess monocyte activation.

Main Results:

  • HIV-1 infection is associated with a proportional increase in nonclassic (CD14(+)CD16(++)) and intermediate (CD14(++)CD16(+)) monocytes.
  • These activated monocytes express high levels of tissue factor and CD62P, correlating with HIV-1 viral load, T-cell activation, and IL-6 levels.
  • In vitro, HIV-1 selectively activated nonclassic monocytes, while LPS activated all subsets; the monocyte activation profile in uncontrolled HIV-1 disease resembles that of ACS.

Conclusions:

  • Immune activation and inflammation in HIV-1 disease significantly alter monocyte subpopulations and their activation phenotypes.
  • These alterations contribute to a pro-atherothrombotic state, thereby increasing cardiovascular risk in individuals with HIV-1 infection.
  • The findings highlight potential therapeutic targets for mitigating cardiovascular complications in HIV-1 patients.

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