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The Journal of Clinical Investigation logoLink to The Journal of Clinical Investigation
. 1987 Nov;80(5):1317–1321. doi: 10.1172/JCI113208

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

D P Hajjar 1, K B Pomerantz 1, D J Falcone 1, B B Weksler 1, A J Grant 1
PMCID: PMC442386  PMID: 3119662

Abstract

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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