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CMV Escapes!

Address correspondence to M. Kent Froberg, DVM, MD, Department of Pathology and Laboratory Medicine, University of Minnesota–Duluth School of Medicine, 1035 University Drive, Duluth, MN 55812, USA; tel 218 726 7223; fax 218 726 7559; e-mail kfroberg{at}d.umn.edu.

Cytomegalovirus (CMV) is an opportunistic pathogen that establishes life-long latent infection without clinical disease in immunocompetent individuals, but can cause severe illness in newborns, transplant recipients, and patients with HIV. CMV has evolved complex molecular mechanisms to avoid host immune detection and destruction. Collectively these mechanisms have been termed "immunoevasion" or "escapology." Perhaps the most essential mechanism of virus survival within the host is latency, a form of reversible nonproductive infection of host cells by replication-competent virus. During periods of active virus replication, however, there are multiple strategies by which CMV evades host defenses. These include methods referred to as camouflage, which aid the virus in hiding from immune defenses, and those referred to as sabotage, whereby the virus disrupts or manipulates host inflammatory or immune responses. The ultimate pathogen survival strategy, host cell transformation, has been demonstrated in vitro for CMV, but to date has not been demonstrated in vivo. This review surveys the current literature on CMV immunoevasion and suggests a paradigm whereby CMV survives host defenses and contributes to atherogenesis.

Keywords: cytomegalovirus, escapology, immunoevasion, cytokines, atherosclerosis

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