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

• Published in: Blood Vol. 120; no. 23; pp. 4599 - 4608
• Main Authors: Funderburg, Nicholas T., Zidar, David A., Shive, Carey, Lioi, Anthony, Mudd, Joseph, Musselwhite, Laura W., Simon, Daniel I., Costa, Marco A., Rodriguez, Benigno, Sieg, Scott F., Lederman, Michael M.
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 29.11.2012; Americain Society of Hematology; American Society of Hematology
• Subjects: Acute Coronary Syndrome - blood; Acute Coronary Syndrome - complications; Acute Coronary Syndrome - immunology; Adult; Aged; Biological and medical sciences; Cardiology. Vascular system; Coronary heart disease; Female; Flow Cytometry; Heart; Hematologic and hematopoietic diseases; HIV Infections - complications; HIV Infections - immunology; HIV Infections - virology; HIV-1 - immunology; HIV-1 - physiology; Host-Pathogen Interactions - immunology; Human viral diseases; Humans; Immunobiology; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunopathology; Immunophenotyping; Infectious diseases; Interleukin-6 - blood; Interleukin-6 - immunology; Lipopolysaccharide Receptors - blood; Lipopolysaccharide Receptors - immunology; Lipopolysaccharides - blood; Lipopolysaccharides - immunology; Male; Medical sciences; Middle Aged; Monocytes - immunology; Monocytes - metabolism; Receptors, IgG - blood; Receptors, IgG - immunology; Thromboplastin - immunology; Thromboplastin - metabolism; Viral diseases; Viral diseases of the lymphoid tissue and the blood. Aids; Young Adult; Human; Immunopathology; Hematology; Immunophenotype; HIV-1 virus; Retroviridae; Cardiovascular disease; AIDS; Coronary heart disease; Immune deficiency; Lentivirus; Myocardial disease; Infection; Virus; Viral disease; Human immunodeficiency virus; Acute coronary syndrome
• ISSN: 0006-4971; 1528-0020; 1528-0020
• DOI: 10.1182/blood-2012-05-433946

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.