HIV and Cardiovascular Diseases Risk: Exploring the Interplay between T cell Activation, Coagulation, Monocyte Subsets and Lipid Subclass Alterations.

This study therefore evaluated T cell-mediated changes and coagulation markers in HIV-positive individuals to ascertain their potential to increase CVD risk. Eighty participants were recruited (Worcester, South Africa) and fasted blood collected to evaluate: a) immune activation (CD38 expression on CD4 and CD8 T cells) and thrombus formation (tissue factor [CD142]) on CD4 and CD8 T cells; b) monocyte subpopulations (non-classical, intermediate, classical) and; and c) classical regulatory T (Treg) cells with activation markers (glycoprotein A repetitions predominant [GARP], special AT-rich sequence-binding protein 1[SATB-1]). High-and low-density lipoprotein subclasses (Lipoprint) were also determined. This study revealed four key findings for HIV-positive patients: a) co-expression of the CD142 coagulation marker together with immune activation on both CD4 and CD8 T cells during chronic infection stages; b) Treg cell activation and upregulated GARP and SATB-1 contributing to Treg dysfunction in chronic HIV; c) Pro-atherogenic monocyte subset expansion with significant correlation between T cell activation and macrophage activation (marker: CD163); and d) significant correlation between immune activation and lipid subclasses, revealing crucial changes that can be missed by traditional lipid marker assessments (LDL, HDL). These data also implicate lipopolysaccharide-binding protein (LBP) as a crucial link between immune activation, lipid alterations and increased CVD risk. ...
Source: American Journal of Physiology. Heart and Circulatory Physiology - Category: Physiology Authors: Tags: Am J Physiol Heart Circ Physiol Source Type: research