Shared Monocyte Subset Phenotypes in HIV-1 Infection and in Uninfected Subjects with Acute Coronary Syndrome

Overview

Journal Blood

Publisher Elsevier

Specialty Hematology

Date 2012 Oct 16

PMID 23065151

Citations 140

Authors

Nicholas T Funderburg

David A Zidar

Carey Shive

Anthony Lioi

Joseph Mudd

Laura W Musselwhite

Daniel I Simon

Marco A Costa

Benigno Rodriguez

Scott F Sieg

Michael M Lederman

Affiliations

Soon will be listed here.

Abstract

The mechanisms responsible for increased cardiovascular risk associated with HIV-1 infection are incompletely defined. Using flow cytometry, in the present study, we examined activation phenotypes of monocyte subpopulations in patients with HIV-1 infection or acute coronary syndrome to find common cellular profiles. Nonclassic (CD14(+)CD16(++)) and intermediate (CD14(++)CD16(+)) monocytes are proportionally increased and express high levels of tissue factor and CD62P in HIV-1 infection. These proportions are related to viremia, T-cell activation, and plasma levels of IL-6. In vitro exposure of whole blood samples from uninfected control donors to lipopolysaccharide increased surface tissue factor expression on all monocyte subsets, but exposure to HIV-1 resulted in activation only of nonclassic monocytes. Remarkably, the profile of monocyte activation in uncontrolled HIV-1 disease mirrors that of acute coronary syndrome in uninfected persons. Therefore, drivers of immune activation and inflammation in HIV-1 disease may alter monocyte subpopulations and activation phenotype, contributing to a pro-atherothrombotic state that may drive cardiovascular risk in HIV-1 infection.

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