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  • Oral presentation
  • Open Access

yesHIV Impairs Reverse Cholesterol Transport from Macrophages: A Possible Mechanism of Atherogenic Effect of HIV-1 Infection

  • 1,
  • 2,
  • 1,
  • 1,
  • 3,
  • 2 and
  • 1Email author
Retrovirology20052 (Suppl 1) :S151

  • Published:


  • Cholesterol
  • Coronary Artery Disease
  • Atherosclerotic Plaque
  • Foam Cell
  • Cholesterol Efflux

Both asymptomatic HIV-1 infection and AIDS are consistently associated with increased risk of coronary artery disease (CAD). The accumulation of cholesterol-loaded 'foam cells' (macrophages) in the walls of arteries is a characteristic feature of atherosclerosis. Here we demonstrate that HIV-1 infection of macrophages leads to impairment of apoA-I-dependent cholesterol efflux, accumulation of cholesterol and formation of foam cells. This effect is mediated by the HIV-1 protein Nef. Transfection of RAW cells with the Nef-expressing plasmid resulted in reduction of efflux and cholesterol accumulation. Nef impaired activity of ABCA1, the main transporter of cholesterol to apoA-I. The role of HIV-infected macrophages in atherosclerosis was supported by the presence of HIV-positive foam cells in atherosclerotic plaques of HIV-infected patients. These results suggest a mechanism by which HIV-infected macrophages may contribute to atherosclerotic plaque formation.


Authors’ Affiliations

Department of Microbiology & Tropical Medicine, The George Washington University, Washington, DC, USA
Baker Heart Research Institute, Melbourne, Victoria, Australia
University of New South Wales, Sydney, NSW, Australia


© The Author(s) 2005