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PLoS One. 2019 Apr 18;14(4):e0215620. doi: 10.1371/journal.pone.0215620. eCollection 2019.

HIV disease, metabolic dysfunction and atherosclerosis: A three year prospective study.

Author information

1
Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
2
Department of Microbiology, Immunology and Tropical Diseases, George Washington University, Washington, DC, United States of America.
3
The Heart Centre, Alfred Hospital, Melbourne, VIC, Australia.
4
HIV and STD Unit, Infectious Disease Service, Hospital Universitari de Bellvitge, Instituto de Investigación Biomédica de Bellvitge, Hospitalet de Llobregat, Barcelona, Spain.
5
Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, VIC, Australia.
6
Department of Infectious Diseases, Alfred Hospital, Melbourne, VIC, Australia.
7
Division of Infectious Diseases, Department of Medicine, George Washington University, Washington, DC, United States of America.
8
Lipid Metabolism Unit, Centre for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States of America.
9
Department of Medicine, Monash University, Melbourne, VIC, Australia.

Abstract

HIV infection is known to be associated with cardiometabolic abnormalities; here we investigated the progression and causes of these abnormalities. Three groups of participants were recruited: HIV-negative subjects and two groups of treatment-naïve HIV-positive subjects, one group initiating antiretroviral treatment, the other remaining untreated. Intima-media thickness (cIMT) increased in HIV-positive untreated group compared to HIV-negative group, but treatment mitigated the difference. We found no increase in diabetes-related metabolic markers or in the level of inflammation in any of the groups. Total cholesterol, low density lipoprotein cholesterol and apoB levels were lower in HIV-positive groups, while triglyceride and Lp(a) levels did not differ between the groups. We found a statistically significant negative association between viral load and plasma levels of total cholesterol, LDL cholesterol, HDL cholesterol, apoA-I and apoB. HIV-positive patients had hypoalphalipoproteinemia at baseline, and we found a redistribution of sub-populations of high density lipoprotein (HDL) particles with increased proportion of smaller HDL in HIV-positive untreated patients, which may result from increased levels of plasma cholesteryl ester transfer protein in this group. HDL functionality declined in the HIV-negative and HIV-positive untreated groups, but not in HIV-positive treated group. We also found differences between HIV-positive and negative groups in plasma abundance of several microRNAs involved in lipid metabolism. Our data support a hypothesis that cardiometabolic abnormalities in HIV infection are caused by HIV and that antiretroviral treatment itself does not influence key cardiometabolic parameters, but mitigates those affected by HIV.

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