Shared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndrome.


Journal Article

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.

Full Text

Cited Authors

  • Funderburg, NT; Zidar, DA; Shive, C; Lioi, A; Mudd, J; Musselwhite, LW; Simon, DI; Costa, MA; Rodriguez, B; Sieg, SF; Lederman, MM

Published Date

  • November 2012

Published In

Volume / Issue

  • 120 / 23

Start / End Page

  • 4599 - 4608

PubMed ID

  • 23065151

Pubmed Central ID

  • 23065151

Electronic International Standard Serial Number (EISSN)

  • 1528-0020

International Standard Serial Number (ISSN)

  • 0006-4971

Digital Object Identifier (DOI)

  • 10.1182/blood-2012-05-433946


  • eng