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

TitleHerpes simplex virus infection in human arterial cells. Implications in arteriosclerosis.
Publication TypeJournal Article
Year of Publication1987
AuthorsHajjar DP, Pomerantz KB, Falcone DJ, Weksler BB, Grant AJ
JournalJ Clin Invest
Volume80
Issue5
Pagination1317-21
Date Published1987 Nov
ISSN0021-9738
KeywordsAnimals, Arachidonic Acid, Arachidonic Acids, Arteries, Arteriosclerosis, Cattle, Cells, Cultured, Cholesterol Esters, Epoprostenol, Herpes Simplex, Humans, L-Lactate Dehydrogenase, Lipid Metabolism, Muscle, Smooth, Vascular, Sterol Esterase, Triglycerides
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.

DOI10.1172/JCI113208
Alternate JournalJ Clin Invest
PubMed ID3119662
PubMed Central IDPMC442386
Grant ListHL-07423 / HL / NHLBI NIH HHS / United States
HL-18828 / HL / NHLBI NIH HHS / United States
HL-35564 / HL / NHLBI NIH HHS / United States
Related Faculty: 
David P. Hajjar, Ph.D. Domenick J. Falcone, Ph.D.

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