Sphingolipid Metabolism during Infection of Human Fibroblasts by Herpes Simplex Virus Type 1

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Abstract
Results from several experiments support the view that sphingomyelin turnover and glycosphingolipid synthesis play a role in herpes simplex virus infection of human skin fibroblast cells in culture. Inhibition of sphingomyelinase by phosphatidylcholine or by a synthetic ceramide, N-palmitoyl-DL-dihydrosphingosine, interferes substantially with virus reproduction as does a genetic defect in the enzyme (Niemann-Pick disease). In Niemann-Pick cells, yields of infectious virus are .apprx. 3% of the normal level. An inhibitor of ceramide:UDP glucose glycosyltransferase was also used to test the effect of altered glycosphingolipid synthesis on infection. This compound, DL-2-decanoylamino-3-morpholinopropiophenone, decreased virus yields to a level .apprx. 0.1% of normal at the highest concentration tested.