Incorporation of 32P-phosphate into membrane phospholipids during infection of cultured human fibroblasts by herpes simplex virus type 1.
Infection of cultured human skin fibroblasts by herpes simplex virus leads to increased incorporation of labeled inorganic phosphate into host membrane sphingomyelin. Incorporation into the other major membrane phospholipids, including phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol and phosphatidylserine, was unaffected. Since sphingomyelin has been shown to serve as precursor to ceramides (via sphingomyelinase) in monkey kidney cells and since enhanced synthesis of ceramide-based glycolipids has been shown to occur after herpes simplex virus infection, we suggest that the observed increase in labeling of sphingomyelin may reflect mobilization for glycolipid synthesis. The distribution of phosphate label among the phospholipids of the viral envelope was identical to that among the phospholipids of the cellular cytoplasmic membrane fraction and differed from that of the nuclear fraction.
D002478:Cells, Cultured; D005227:Fatty Acids / Q000378:metabolism; D005347:Fibroblasts; D006801:Humans; D008563:Membrane Lipids / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism*; D010743:Phospholipids / Q000378:metabolism*; D018139:Simplexvirus / Q000254:growth & development*; D012867:Skin; D013109:Sphingomyelins / Q000378:metabolism
D005227:Fatty Acids; D008563:Membrane Lipids; D010710:Phosphates; D010743:Phospholipids; D013109:Sphingomyelins