Abstract
BackgroundIncreased prevalence of atherosclerotic cardiovascular disease in HIV-infected patients has been observed. The cause of this accelerated atherosclerosis is a matter of controversy. As clinical studies are complicated by a multiplicity of risk-factors and a low incidence of hard endpoints, studies in animal models could be attractive alternatives.Methodology/Principal FindingsWe evaluated gene expression of lectin-like oxidized-low-density-lipoprotein receptor-1 (LOX-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in HIV-1 transgenic (HIV-1Tg) rats; these genes are all thought to play important roles in early atherogenesis. Furthermore, the plasma level of sICAM-1 was measured. We found that gene expressions of LOX-1 and VCAM-1 were higher in the aortic arch of HIV-1Tg rats compared to controls. Also, the level of sICAM-1 was elevated in the HIV-1Tg rats compared to controls, but the ICAM-1 gene expression profile did not show any differences between the groups.Conclusions/SignificanceHIV-1Tg rats have gene expression patterns indicating endothelial dysfunction and accelerated atherosclerosis in aorta, suggesting that HIV-infection per se may cause atherosclerosis. This transgenic rat model may be a very promising model for further studies of the pathophysiology behind HIV-associated cardiovascular disease.
Highlights
The morbidity and mortality among patients with human immunodeficiency virus (HIV) infection has declined dramatically since the introduction of antiretroviral therapy (ART)
In HIV-1 transgenic (HIV-1Tg) rats the gene expression level for vascular cell adhesion molecule-1 (VCAM-1) was higher in the aortic arch compared to the abdominal aorta (1.9fold, p = 0.011)
There were no significant differences in intercellular adhesion molecule-1 (ICAM-1) gene expression between HIV-1Tg and control rats (Fig. 1C)
Summary
The morbidity and mortality among patients with human immunodeficiency virus (HIV) infection has declined dramatically since the introduction of antiretroviral therapy (ART). Increased rates of atherosclerotic cardiovascular disease in HIV-infected patients have been observed. The cause of accelerated atherosclerosis behind most cardiovascular diseases, developed by HIV-patients, is still a matter of controversy. Three possibilities have been suggested: the infection itself, the treatment used or the dyslipidemia often seen in HIV-patients [1,2]. As it is not possible to totally isolate the different causes in clinical experiments, an animal model represents an attractive alternative to investigate in detail the origin of accelerated atherosclerosis associated with HIV-infection per se. Increased prevalence of atherosclerotic cardiovascular disease in HIV-infected patients has been observed. The cause of this accelerated atherosclerosis is a matter of controversy. As clinical studies are complicated by a multiplicity of risk-factors and a low incidence of hard endpoints, studies in animal models could be attractive alternatives
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