It was found that HIV-1 Tat protein (therefore HIV itself) induced the expression of ICAM-1 and VCAM-1 and this could be a possible mechanism by which HIV-1 infection contributes to endothelial injury and accelerated atherosclerosis.35,36 It could therefore be expected that the HIV-infected, never antiretroviral-treated participants with definite signs of endothelial injury would also show signs of endothelial dysfunction. This evidence concerns the gene VCAM1 and endothelial dysfunction.