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

Hann Low, Anh Hoang, Tatiana Pushkarsky, Larisa Dubrovsky, Elizabeth Dewar, Maria Silvana Di Yacovo, Nigora Mukhamedova, Lesley Cheng, Catherine Downs, Gary Simon, Maria Saumoy, Andrew F. Hill, Michael L. Fitzgerald, Paul Nestel, Anthony Dart, Jennifer Hoy, Michael Bukrinsky, Dmitri Sviridov

Research output: Contribution to journalArticleResearchpeer-review

3 Citations (Scopus)

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.

Original languageEnglish
Article numbere0215620
Number of pages19
JournalPLoS ONE
Volume14
Issue number4
DOIs
Publication statusPublished - 1 Apr 2019

Cite this