Date Published: January 30, 2007
Publisher: PLoS Medicine
Author(s): Michael Bukrinsky, Dmitri Sviridov
Partial Text: In their Perspective published in PLoS Medicine , Carr and Ory provide a fair review of our recent paper in PLoS Biology . However, we believe their commentary puts too much emphasis on the role of low high-density lipoprotein (HDL) cholesterol levels as a cause of atherosclerosis in HIV-infected patients. While HDL cholesterol levels are reduced in untreated HIV infection , and defects in reverse cholesterol transport (RCT) that we reported may well be a contributing factor to this abnormality, initiation of antiretroviral therapy restores HDL levels . Although the development of dyslipidemia with prolonged use of anti-HIV drugs again lowers HDL cholesterol and in addition raises very low-density lipoprotein and low-density lipoprotein levels , it is unlikely that HIV infection contributes significantly to these effects. Indeed, most HDL comes from the liver and intestine, which are responsible for maintaining plasma HDL levels , but neither hepatocytes nor enterocytes are infected by HIV. Also, the number of HIV-infected cells in treated patients is relatively low to account for any general changes in concentration of plasma lipoproteins.