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Isolation, Transfection, and Culture of Primary Human Monocytes
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Increased CD36 expression on circulating monocytes during HIV infection.

Luca Meroni1, Agostino Riva, Paola Morelli

  • 1Institute of Infectious Diseases and Tropical Medicine, Luigi Sacco Hospital, University of Milan, Milan, Italy. luca.meroni@unimi.it

Journal of Acquired Immune Deficiency Syndromes (1999)
|March 1, 2005
PubMed
Summary

HIV-1 infection significantly increases CD36 expression on monocytes, a receptor involved in lipid metabolism. This elevated CD36 may contribute to atherosclerosis risk in HIV patients, independent of antiretroviral therapy.

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Area of Science:

  • Immunology
  • Metabolic Research
  • HIV/AIDS Research

Background:

  • Metabolic alterations and abnormal fat distribution are common in HIV-1 patients on antiretroviral therapy.
  • CD36, a receptor crucial for lipid uptake and metabolism, has wide tissue distribution.

Purpose of the Study:

  • To quantify CD36 expression on monocytes in HIV-1 patients versus healthy controls.
  • To correlate CD36 levels with metabolic and immunovirologic markers.

Main Methods:

  • Flow cytometry was used to measure CD36 expression on monocytes from 165 HIV-1 patients and 35 healthy controls.
  • Statistical analyses included univariate and multivariate analysis of variance.

Main Results:

  • CD36 expression was significantly higher in HIV-1 patients compared to controls (P < 0.0001).
  • HIV-1 infection was the sole predictor of CD36 expression in multivariate analysis.
  • No correlation was observed between CD36 levels and age, sex, BMI, lipid levels, HIV RNA, or antiretroviral treatment parameters.

Conclusions:

  • HIV-1 infection is linked to elevated CD36 expression on circulating monocytes.
  • Antiretroviral drugs have a minimal impact on CD36 homeostasis.
  • Increased monocyte CD36 may indicate a proatherogenic state in HIV-infected individuals.