title: Herpes simplex virus infection in human arterial cells. Implications in arteriosclerosis.
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.
mesh_terms: D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects / Q000378:metabolism; D001161:Arteriosclerosis / Q000209:etiology*; D002417:Cattle; D002478:Cells, Cultured; D002788:Cholesterol Esters / Q000378:metabolism; D011464:Epoprostenol / Q000096:biosynthesis; D006561:Herpes Simplex / Q000378:metabolism*; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D050356:Lipid Metabolism; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D002787:Sterol Esterase / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
chemical_list: D001095:Arachidonic Acids; D002788:Cholesterol Esters; D014280:Triglycerides; D016718:Arachidonic Acid; D011464:Epoprostenol; D007770:L-Lactate Dehydrogenase; D002787:Sterol Esterase