There is some indication of a possible direct effect from viral protein particles orinfected cells liberating proteins in the receptors present in the vascularendothelium, thus favoring the presence of pro-coagulants, platelet activation,reduced nitric oxide production from the destruction of CD4 T lymphocytes(CD4+ cell), and the production of inflammatory cytokines.4,9,10 Recentpublications have indicated that viral effect on the vascular endothelium cancontribute to a reduction in the number of primary endothelial cells, which leads toendothelial dysfunction and atherosclerosis.11 Here, CD4 is linked to atherosclerosis.