|Title||Herpes simplex virus infection in human arterial cells. Implications in arteriosclerosis.|
|Publication Type||Journal Article|
|Year of Publication||1987|
|Authors||Hajjar DP, Pomerantz KB, Falcone DJ, Weksler BB, Grant AJ|
|Journal||J Clin Invest|
|Date Published||1987 Nov|
|Keywords||Animals, 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|
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.
|Alternate Journal||J Clin Invest|
|PubMed Central ID||PMC442386|
|Grant List||HL-07423 / HL / NHLBI NIH HHS / United States |
HL-18828 / HL / NHLBI NIH HHS / United States
HL-35564 / HL / NHLBI NIH HHS / United States
Domenick J. Falcone, Ph.D.