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There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
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Advisor, Rudolph L. Gleason, Jr., PhD
Dr. Manu Platt (Georgia Tech)
Dr. W Robert Taylor (GT / Emory)
Dr. Hanjoong Jo (GT / Emory)
Dr. Roy Sutliff (Emory)
Since the development of highly active antiretroviral therapy (HAART), patients infected with human immunodeficiency virus (HIV-1) have been living longer lives. HIV-1+ populations are experiencing early onset cardiovascular disease (CVD) including myocardial infarction, atherosclerotic lesions, and other subclinical markers of atherosclerosis. The mechanisms of CVD progression have been linked to HAART, HIV-1 infection, or both. Thus, there is a pressing need to investigate the mechanisms of these drugs in CVD progression. The goal of this proposal is to perform parallel clinical and experimental studies to parse out the underlying mechanisms of CVD progression with HIV-1 infection and HAART. The central hypothesis is that HAART drugs and HIV infection will induce endothelial dysfunction, carotid intima-media thickening, and arterial stiffening. Preliminary data suggest that HAART drugs have negative effects on cIMT, elastic modulus, and brachial flow-mediated dilation. Mice will be exposed to HAART drugs, and analyses will be performed on the vasculature to examine reactive oxygen species, endothelial dysfunction, and alterations in the mechanical properties of the vessels. By utilizing models that incorporate dyslipidemia and altered flow, we will be able to identify mechanisms that are specific to HAART drugs, lipids, and flow in order to suggest an efficacious mode of intervention.
