Abstract
HIV-infected subjects are at high risk of developing atherosclerosis, in part due to virus-induced impairment of HDL metabolism. Here, using as a model of HIV infection the NOD.Cg-Prkdc scidIL2rg tm1Wjl/SzJ (NSG) mice humanized by human stem cell transplantation, we demonstrate that LXR agonist TO901317 potently reduces viral replication and prevents HIV-induced reduction of plasma HDL. These results establish that humanized mice can be used to investigate the mechanisms of HIV-induced impairment of HDL formation, a major feature of dyslipidemia associated with HIV-1 infection, and show potential benefits of developing LXR agonists for treatment of HIV-associated cardio-vascular disease.
Original language | English |
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Pages (from-to) | 95-98 |
Number of pages | 4 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 419 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2 Mar 2012 |
Externally published | Yes |
Keywords
- Atherosclerosis
- HIV-1
- Humanized mice
- Liver X receptor agonist
- Pathogenesis