Herpesviruses in Atherosclerosis and Thrombosis

Etiologic Agents or Ubiquitous Bystanders?

From the Departments of Pathology (A.C.N., D.P.H.) and Biochemistry (D.P.H.), Center of Vascular Biology, Cornell University Medical College, New York, NY.

Correspondence to David P. Hajjar, Departments of Pathology and Biochemistry, Center of Vascular Biology, Cornell University Medical College, 1300 York Ave, New York, NY 10021. E-mail dphajjar{at}mail.med.cornell.edu

Abstract

Abstract—The role of herpesvirus infections in the pathogenesis of vascular diseases remains an enigma. Although there is abundant circumstantial evidence of a role for herpesviruses in atherosclerosis and related processes, a cause-and-effect relationship has yet to be definitively established. This article will review the pathological, molecular, and biochemical evidence supporting the hypothesis that herpesviruses are involved in the development of atherosclerosis, restenosis after coronary angioplasty, accelerated atherosclerosis in recipients of heart transplants, and the induction of a prothrombotic phenotype in vascular endothelial cells.

Key Words: herpesviruses • atherosclerosis • thrombosis • endothelium • vascular smooth muscle cell

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