Volume 2 Supplement 1

2005 International Meeting of The Institute of Human Virology

Open Access

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

  • Zahedi Mujawar1,
  • Honor Rose2,
  • Matthew P Morrow1,
  • Jan Orenstein1,
  • Yuri Bobryshev3,
  • Dmitri Sviridov2 and
  • Michael Bukrinsky1Email author
Retrovirology20052(Suppl 1):S151


Published: 8 December 2005

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
Baker Heart Research Institute
University of New South Wales


© The Author(s) 2005