HIV infection and high density lipoprotein metabolism

Abstract

HIV infection and its treatment are associated with dyslipidemia, including hypoalphalipoproteinemia, and increased risk of cardiovascular disease. Parameters of HDL metabolism in HIV-positive patients were investigated in a cross-sectional study. The following groups of subjects were selected: i) 25 treatment-naïve HIV-infected patients or HIV-infected patients on long therapy break, ii) 28 HIV-infected patients currently treated with protease inhibitors, and iii) 33 HIV-negative subjects. Compared to the HIV-negative group, all groups of HIV-infected patients were characterized by significantly elevated triglyceride and apolipoprotein B levels, mass and activity of lecithin cholesterol acyl transferase and cholesteryl ester transfer protein (p<0.01). Total and LDL cholesterol was lower in treatment-naïve HIV-infected group only. HDL cholesterol and preβ 1 -HDL were significantly lower in all HIV-infected groups (p<0.05), while mean levels of apolipoprotein A-I (apoA-I) and ability of plasma to promote cholesterol efflux were similar in all groups. We found a positive correlation between apoA-I and levels of CD4+ cells (r 2 = 0.3, p<0.001). Plasma level of phospholipid transfer protein was reduced in the group on antiretroviral therapy. Taken together these results suggest that HIV infection is associated with modified HDL metabolism re-directing cholesterol to the apoB-containing lipoproteins and likely reducing the functionality of reverse cholesterol transport.

HDL in Infectious Diseases and Sepsis

“…Not all data are however concordant on this, and although HDL cholesterol and preβ1-HDL were significantly lower in all HIV-infected groups ( p < 0.05), mean levels of apoA-I and the ability of plasma to promote cholesterol efflux were similar in treatment-naïve HIV-infected patients or in HIV-infected patients on long therapy break. Of note a positive correlation between apoA-I and levels of CD4+ cells was also observed (r 2 ¼ 0.3, p < 0.001) (Rose et al 2008). Furthermore apoA-I, the major protein component of high-density lipoprotein, and its amphipathic peptide analogue were found to inhibit cell fusion, both in HIV-1-infected T cells and in recombinant vaccinia-virus-infected CD4+ HeLa cells expressing HIV envelope protein on their surfaces (Srinivas et al 1990).…”

“…In vitro, these abnormalities were significantly improved by treatment with the apoA-1 mimetic peptide 4F (Kelesidis et al 2011). HIV infection is associated with modified HDL metabolism redirecting cholesterol to the apoBcontaining lipoproteins and likely reducing the functionality of reverse cholesterol transport (Rose et al 2008). Of note, the HIV-1 Nef protein can impair ABCA1 cholesterol efflux from macrophages, thus supporting atherosclerosis.…”

Use of HMG-CoA Reductase Inhibitors in the HIV Population: Implications for Individualized Treatment Selection

“…Participants were assigned to 1 of 4 study groups: HIV-negative (n = 33), HIV-infected treatment naïve (n = 11), HIV-infected currently untreated (n = 14), or HIV-infected with PI treatment (n = 28). 9 TC and LDL-C were significantly lower in the HIV-infected treatment-naïve group compared with each of the other 3 study groups. Triglycerides were significantly lower, and HDL-C was significantly higher in the HIV-negative group compared with each of the other 3 study groups.…”

“…Triglycerides were significantly lower, and HDL-C was significantly higher in the HIV-negative group compared with each of the other 3 study groups. 9 A retrospective cohort analysis compared the mean age at diagnosis, incidence rates (IR), and adjusted incidence rates (aIR) by HIV status for myocardial infarction (MI), end-stage renal disease (ESRD), and non-AIDS-defining cancer. The study population included patients from the Veterans Aging Cohort Study who were matched 1 HIV-positive to 2 HIVnegative by age, race, and clinical site from October 2003 to September 2008.…”

Pattern of dyslipidaemia in human immunodeficiency virus infected patients- a study from rural tertiary care hospital in central India

“…14 Multiple pathogenic mechanisms by which HIV virus leads to dyslipidaemia have been hypothesized but they are still controversial. [14][15][16][17][18][19] Patient of HIV have two fold increased risk of MI compared with those without HIV infection and this is attributed to the metabolic alteration due to HIV itself, dyslipidaemia and increasing age due to increased longevity. 20 There were several studies done for the prevalence and pattern of dyslipidaemia in HIV patient but most of them were conducted in urban setting and there was no study done from central India in rural set up to show the lipid profile in HIV patient, therefore this study was undertaken to find out lipid profile in HIV patient across different stages of HIV/AIDS.…”