Herpes simplex virus infection in human arterial cells. Implications in arteriosclerosis.

D P Hajjar; K B Pomerantz; D J Falcone; B B Weksler; A J Grant

doi:10.1172/JCI113208

Department of Biochemistry, National Institutes of Health Specialized Center for Research in Thrombosis, Cornell University Medical College, New York, New York 10021.

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Department of Biochemistry, National Institutes of Health Specialized Center for Research in Thrombosis, Cornell University Medical College, New York, New York 10021.

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Department of Biochemistry, National Institutes of Health Specialized Center for Research in Thrombosis, Cornell University Medical College, New York, New York 10021.

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Department of Biochemistry, National Institutes of Health Specialized Center for Research in Thrombosis, Cornell University Medical College, New York, New York 10021.

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Department of Biochemistry, National Institutes of Health Specialized Center for Research in Thrombosis, Cornell University Medical College, New York, New York 10021.

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Published in Volume 80, Issue 5 on November 1, 1987
J Clin Invest. 1987;80(5):1317–1321. https://doi.org/10.1172/JCI113208.
© 1987 The American Society for Clinical Investigation

Published November 1, 1987 - Version history

Herpesviruses have been implicated as etiologic factors in the pathogenesis of human arteriosclerosis. We have examined the pathobiological effects of human herpes simplex virus (HSV-1) infection in influencing lipid accumulation and metabolism in human and bovine arterial smooth muscle cells (SMC). Significantly greater amounts of saturated cholesteryl esters (CE) and triacylglycerols (TG) accumulate in HSV-1-infected human and bovine arterial SMC than uninfected cells. This CE accumulation results, in part, from decreased CE hydrolysis. Furthermore, arachidonate-stimulated, HSV-1-infected arterial SMC have a reduced capacity to produce prostacyclin (an agonist of intracellular CE hydrolytic activity) than uninfected, stimulated SMC. It appears that HSV-1 may induce lipid accumulation in arterial SMC similar, in part, to the lipid accumulation observed in vivo during human atherogenesis. Thus, herpesviruses may contribute to lipid accumulation, which is a characteristic feature of atherosclerosis.