ABSTRACT
HIV-1 cardiomyopathy (HIVCM) is an increasing cause of cardiovascular morbidity and mortality in young and middle-aged HIV-1-positive adults surviving acute complications of AIDS (1,2). It is controversial whether HIV-1 per se, opportunistic viral infections, substance abuse, and/or highly active antiretroviral therapy (HAART) is primarily responsible for HIVCM. Although HIV-1 is clearly an etiological factor in HIVCM, the role of HIV-1 proteins, which are considered important in HIV-1 encephalitis [i.e. gp120 (3,4), Tat (5), and Nef (4)] have not been clarified in HIVCM. We have investigated HIV-1 entry and apoptosis in human coronary artery endothelial cells and neonatal rat myocytes in vitro and in heart tissues of patients with AIDS ex vivo. Our data indicate that HIV-1 invades the heart and brain by a transcellular route through coronary artery endothelial cells (CAECs) or brain microvascular endothelial cells (BMVECs), respectively, using the mechanism of macropinocytosis. In the myocardium, HIV-1 infects macrophages and lymphocytes and induces cardiomyocyte apoptosis and heart failure.
