Sphingolipid metabolism during infection of human fibroblasts by herpes simplex virus type 1.
Results from several experiments support the view that sphingomyelin turnover and glycosphingolipid synthesis play a role in herpes simplex virus infection of 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 about 3% of the normal level. An inhibitor of ceramide: UDP glucose glucosyltransferase 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 about 0.1% of normal at the highest concentration tested.
D002478:Cells, Cultured; D005347:Fibroblasts / Q000378:metabolism; D005964:Glucosyltransferases / Q000037:antagonists & inhibitors; D006028:Glycosphingolipids / Q000096:biosynthesis; D006561:Herpes Simplex / Q000378:metabolism*; D006801:Humans; D018139:Simplexvirus; D013107:Sphingolipids / Q000378:metabolism*; D013108:Sphingomyelin Phosphodiesterase / Q000037:antagonists & inhibitors; D013109:Sphingomyelins / Q000378:metabolism; D014779:Virus Replication
D006028:Glycosphingolipids; D013107:Sphingolipids; D013109:Sphingomyelins; D005964:Glucosyltransferases; D013108:Sphingomyelin Phosphodiesterase