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Project leader: Dr Nigora Mukhamedova

Cardiovascular disease (CVD) contributes substantially to the overall morbidity of HIV-infected individuals, as 10 to 30 per cent of these subjects are presented with some form of CVD. The main underlying cause of CVD is atherosclerosis, and factors that are epidemiologically and prospectively the strongest predictors of atherosclerosis are dyslipidemia and impairment of intracellular cholesterol metabolism. Dyslipidemia in HIV-infected patients has been attributed mainly to antiretroviral drugs, in particular protease inhibitors. Our recent studies suggest that HIV infection impairs intracellular cholesterol metabolism and thus itself is a potent pro-atherogenic factor. This finding may have profound implications for treatment strategy. Indeed, if HIV triggers or continuously causes pro-atherogenic changes, the timely treatment of HIV infection may be essential for prevention of cardiovascular complications.

Our studies in collaboration with George Washington University, Washington, DC, USA, have suggested that HIV impairs reverse cholesterol transport and metabolism of high density lipoprotein (HDL) and that may be the key mechanism connecting HIV to atherosclerosis. We are currently conducting a study to characterize changes in structure, metabolism and functionality of HDL associated with HIV-1 infection, and to correlate them with the surrogate measures of progression of atherosclerosis in HIV-infected patients. We also investigate the cellular mechanisms responsible for the impairment of cholesterol metabolism due to HIV infection.

A connection between infection and cardiovascular and metabolic diseases may not be limited to HIV infection. We are conducting a collaborative study with La Trobe University and Karolinska Institute in Stockholm, Sweden to investigate an impairment of cholesterol metabolism by cytomegalovirus and by the most primitive infection, prions.

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