HIV/hepatitis C virus coinfection ameliorates the atherogenic lipoprotein abnormalities of HIV infection

Abstract

Higher levels of small low-density lipoprotein (LDL) and lower levels of high-density lipoprotein (HDL) subclasses have been associated with increased risk of cardiovascular disease. The extent to which HIV infection and HIV/hepatitis C virus (HCV) coinfection are associated with abnormalities of lipoprotein subclasses is unknown. Lipoprotein subclasses were measured by nuclear magnetic resonance (NMR) spectroscopy in plasma samples from 569 HIV-infected and 5948 control participants in the Fat Redistribution and Metabolic Change in HIV Infection (FRAM), Coronary Artery Risk Development in Young Adults (CARDIA), and Multi-Ethnic Study of Atherosclerosis (MESA) studies. Multivariable regression was used to estimate the association of HIV and HIV/HCV coinfection with lipoprotein measures with adjustment for demographics, lifestyle factors, and waist-to-hip ratio. Relative to controls, small LDL levels were higher in HIV-monoinfected persons (+381 nmol/l, P <0.0001), with no increase seen in HIV/HCV coinfection (-16.6 nmol/l). Levels of large LDL levels were lower (-196 nmol/l, P <0.0001) and small HDL were higher (+8.2 μmol/l, P < 0.0001) in HIV monoinfection with intermediate values seen in HIV/HCV coinfection. Large HDL levels were higher in HIV/HCV-coinfected persons relative to controls (+1.70 μmol/l, P <0.0001), whereas little difference was seen in HIV-monoinfected persons (+0.33, P = 0.075). Within HIV-infected participants, HCV was associated independently with lower levels of small LDL (-329 nmol/l, P <0.0001) and small HDL (-4.6 μmol/l, P <0.0001), even after adjusting for demographic and traditional cardiovascular risk factors. HIV-monoinfected participants had worse levels of atherogenic LDL lipoprotein subclasses compared with controls. HIV/HCV coinfection attenuates these changes, perhaps by altering hepatic factors affecting lipoprotein production and/or metabolism. The effect of HIV/HCV coinfection on atherosclerosis and the clinical consequences of low small subclasses remain to be determined.