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Retrovirology

, 2:S151 | Cite as

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

  • Zahedi Mujawar
  • Honor Rose
  • Matthew P Morrow
  • Jan Orenstein
  • Yuri Bobryshev
  • Dmitri Sviridov
  • Michael Bukrinsky
Open Access
Oral presentation
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Keywords

Cholesterol Coronary Artery Disease Atherosclerotic Plaque Foam Cell Cholesterol Efflux 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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.

Copyright information

© The Author(s) 2005

Authors and Affiliations

  • Zahedi Mujawar
    • 1
  • Honor Rose
    • 2
  • Matthew P Morrow
    • 1
  • Jan Orenstein
    • 1
  • Yuri Bobryshev
    • 3
  • Dmitri Sviridov
    • 2
  • Michael Bukrinsky
    • 1
  1. 1.Department of Microbiology & Tropical MedicineThe George Washington UniversityWashingtonUSA
  2. 2.Baker Heart Research InstituteMelbourneAustralia
  3. 3.University of New South WalesSydneyAustralia

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