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Updated: Feb 20, 2026
Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
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
Insights
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.
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.
Background:
Metabolic alterations and abnormalities of fat distribution are common findings in antiretroviral-treated HIV-1-infected patients. CD36 is a multifunctional receptor with a wide tissue distribution that plays a crucial role in the cellular uptake and metabolism of lipids.
Objectives:
To define the level of CD36 expression on circulating monocytes from HIV-1-infected patients and healthy controls (HCs) and to correlate CD36 expression levels with metabolic and immunovirologic parameters.
Methods:
CD36 expression on peripheral blood monocytes was measured by means of flow cytometry in 165 HIV-1-infected patients and in 35 HCs. Statistical analysis was performed by means of univariate and multivariate analysis of variance models.
Results:
CD36 expression was significantly higher in HIV-1-infected patients compared with HCs (P < 0.0001). HIV-1 infection was the only variable associated with CD36 expression on multivariate analysis, whereas no correlation was found between CD36 level and age, sex, body mass index, lipid serum levels, HIV RNA levels, time on antiretroviral therapy, or kind of antiretroviral regimen.
Conclusions:
HIV-1 infection is associated with increased expression of CD36 on circulating monocytes, and antiretroviral drugs play only a minor role in the complex homeostasis of this receptor. Given its role in the cellular uptake and accumulation of lipids, CD36 increased levels on monocytes could represent a proatherogenic condition in HIV-infected patients.
