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

J Clin Invest. 1987 Nov;80(5):1317-21. doi: 10.1172/JCI113208.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Arachidonic Acid
  • Arachidonic Acids / pharmacology
  • Arteries / drug effects
  • Arteries / metabolism
  • Arteriosclerosis / etiology*
  • Cattle
  • Cells, Cultured
  • Cholesterol Esters / metabolism
  • Epoprostenol / biosynthesis
  • Herpes Simplex / metabolism*
  • Humans
  • L-Lactate Dehydrogenase / metabolism
  • Lipid Metabolism*
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism*
  • Sterol Esterase / metabolism
  • Triglycerides / metabolism


  • Arachidonic Acids
  • Cholesterol Esters
  • Triglycerides
  • Arachidonic Acid
  • Epoprostenol
  • L-Lactate Dehydrogenase
  • Sterol Esterase