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Updated: Oct 3, 2026

Isolation and Identification of Extravascular Immune Cells of the Heart
Published on: August 23, 2018
Essential role of HIV type 1-infected and cyclooxygenase 2-activated macrophages and T cells in HIV type 1
1Department of Medicine, West Los Angeles VA Medical Center and UCLA School of Medicine, Los Angeles, California 90095-1769, USA.
Insights
HIV-1 cardiomyopathy in AIDS patients involves heart muscle inflammation (myocarditis) caused by infected immune cells. Cyclooxygenase-2 (COX-2) activation in these cells is linked to disease progression.
Area of Science:
- Immunology
- Cardiology
- Virology
Background:
- HIV-1 cardiomyopathy is a significant cause of mortality in AIDS patients.
- The precise mechanisms driving HIV-1 cardiomyopathy remain incompletely understood.
Purpose of the Study:
- To investigate the role of immune cell infiltration and specific molecular markers in the pathogenesis of HIV-1 cardiomyopathy.
- To explore the relationship between HIV-1 infection, inflammation, and cardiac dysfunction.
Main Methods:
- Utilized antigen retrieval and immunostaining techniques on cardiac tissue from 15 AIDS patients (3 with dilated cardiomyopathy) and controls.
- Performed immunocytochemistry to identify infiltrating mononuclear cells (macrophages, T cells) and assess tight junction protein (ZO-1) disruption and vascular leakage.
- Examined the expression of HIV-1 peptides (gp120, Nef), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in cardiac cells.
Main Results:
- Identified mononuclear cell infiltrates, including macrophages and T cells (CD3+, CD8+), in the myocardium of AIDS patients, consistent with myocarditis.
- Observed disruption of the tight junction protein ZO-1 and fibrinogen leakage in coronary vessels of AIDS patients, indicating impaired vascular integrity.
- Found a subset of macrophages positive for both COX-2 and iNOS. HIV-1 peptides gp120 and Nef were expressed in macrophages and T cells.
- Correlated higher COX-2 expression and denser inflammatory infiltrates with cardiac failure in AIDS patients.
Conclusions:
- HIV-1-infected monocyte-macrophages and T cells, particularly those with activated COX-2, play a critical role in the progression of HIV-1 myocarditis to cardiomyopathy.
- Impaired vascular integrity and inflammatory responses mediated by these cells contribute to cardiac dysfunction in AIDS.
Abstract:
HIV-1 cardiomyopathy has become a major cause of death in AIDS patients, but its pathogenesis is unclear. We used an antigen retrieval technique and immunostaining to investigate the hearts of 15 AIDS patients, of whom 3 had dilated cardiomyopathy. Immunocytochemistry shows infiltration of the left ventricular myocardium with mononuclear cells, ranging from minimal to diagnostic of myocarditis. The infiltrates include macrophages and CD3(+) and CD8(+) T cells. The tight junction protein ZO-1 is disrupted at the site of monocyte-macrophage vascular penetration and the coronary vessels show fibrinogen leakage in the hearts of AIDS patients, but not in the normal heart. A subset of infiltrating macrophages is doubly positive for cyclooxygenase 2 (COX-2) and inducible nitric oxide synthase. HIV-1 peptides gp120 and Nef are expressed in macrophages and T cells, but not in cardiomyocytes. COX-2 is expressed by both gp120-positive and gp120-negative macrophages. The hearts of AIDS patients separate into those showing minimal infiltrates with low COX-2 expression and those with dense infiltrates and high COX-2; all failing hearts are in the latter group. These data suggest that COX-2-activated and HIV-1-infected monocyte-macrophages and T cells play a crucial role in the progression of HIV-1 myocarditis to HIV-1 cardiomyopathy.
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