The role of infection in restenosis and atherosclerosis: focus on cytomegalovirus  SE Epstein, E Speir, YF Zhou, E Guetta, M Leon, T Finkel  The Lancet  Volume 348, Pages S13-S17 (November 1996) DOI: 10.1016/S0140-6736(96)98005-8 Copyright © 1996 Elsevier Ltd Terms and Conditions

Figure Model of the role of human CMV in restenosis and in atherosclerosis Upper left: recently injured blood vessel wall containing smooth muscle cells (SMCs), with monocytes being attracted to the site of vascular injury (as part of the inflammatory response to injury). Subsets of each cell type are depicted as containing latently infected CMV. Upper right: after vessel injury (either angioplasty-induced or secondary to such risk factors as hypertension, hypercholesterolaemia, or cigarette smoking), CMV is reactivated and expresses its immediate-early genes. Whether it also expresses early and late genes, and whether it replicates, is unclear). The reactivated virus residing in monocytes may infect neighbouring SMCs. Lower centre: through multiple cellular mechanisms, including inactivation of p53, the viral proteins increase neointimal SMC accumulation either by increasing SMC proliferation or by inhibiting SMC apoptosis. The Lancet 1996 348, S13-S17DOI: (10.1016/S0140-6736(96)98005-8) Copyright © 1996 Elsevier Ltd Terms and Conditions