[39] MEASUREMENT OF CD36 EXPRESSION ON MONOCYTES OF LONG-TERM HIGHLY ACTIVE ANTIRETROVIRAL THERAPY-TREATED HIV PATIENTS

5th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV

8–11 July 2003, Le Meridien Montparnasse, Paris, France

MEASUREMENT OF CD36 EXPRESSION ON MONOCYTES OF LONG-TERM HIGHLY ACTIVE ANTIRETROVIRAL THERAPY-TREATED HIV PATIENTS

Antiviral Therapy 2003; 8:L31 (abstract 39)

J Roeling¹, K Wendlandt¹, C Huber², S Hillebrand¹, R Gruber¹, F-D Goebel¹ and B Banas¹
¹Department of Infectious Diseases, Medical Policlinic, University of Munich, Munich, Germany; and ²Department of Virology, Max von Pettenkofer-Institut, University of Munich, Munich, Germany

OBJECTIVES/AIMS: A common side effect of highly active antiretroviral therapy (HAART) is the development of dyslipidaemia, especially in patients on protease inhibitor (PI)-containing regimens. CD36 is a scavenger receptor that is expressed in different cells including monocytes/macrophages and mediates intracellular cholesterol uptake. Recent experimental studies with mouse models have demonstrated that PI therapy leads to an up-regulation of CD36 on macrophages, accumulation of intracellular cholesteryl esters and development of atherosclerotic plaques in different mouse models. In regard to these in vitro experiments, the aim of our study was to examine CD36 expression on peripheral monocytes (MO) in HIV patients receiving long-term antiretroviral therapy.

METHODS: One hundred and fifty patients were studied and three groups were formed divided into low (<200 mg/dl; groups 1,3,5) and high (>200 mg/dl, groups 2, 4, 6) cholesterol: healthy controls (1, 2), HIV patients on HAART without PI (3, 4) and HIV patients on HAART with PI (5, 6). Double-staining of human peripheral blood mononuclear cells (PBMCs) with antibodies against CD36 and a monocyte-marker CD14 by FACS-scan was performed.

RESULTS: Compared to group 1, CD36 expression decreased in groups 3 (–23, 2%) and 5 (–7, 8%), indicating that CD36 is down-regulated in HAART-treated patients with normal cholesterol levels. In the studied high cholesterol groups (2, 4, 6), CD36 levels were lower in groups 4 (–6, 9%) and 6 (–8, 7%) than in group 2. Furthermore, comparing both HAART-treated groups without PI (3, 4), we see no difference in CD36 expression with regard to cholesterol.

CONCLUSIONS/DISCUSSION: As already discussed in the literature, different CD36 expression is seen in macrophages and PBMCs. Our findings show that, in HAART-treated HIV patients, CD36 expression is reduced on patient monocytes. Decreased CD36 expression might lead to impaired cholesterol uptake causing increased serum cholesterol concentration. This in turn might enhance transformation of macrophages to foam cells. In contrast to mouse macrophages, we cannot see an influence of PI on human monocytes. Therefore, further in vitro experiments with HAART-treated macrophages studying the CD36 expression will be performed.

Presenting author: J Roeling

2003-07-08
39

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