Alterations in Glycosphingolipid Patterns in a Line of African Green Monkey Kidney Cells Infected with Herpesvirus

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Abstract
The major glycosphingolipids (GSL) of a line of African green monkey kidney cells (BGM) were characterized as glucosylceramide, lactosylceramide galactosyl-galactosyl-glucosylceramide and N-acetylgalactosaminyl-galactosyl-galactosyl-glucosylceramide. Neutral GSL accounted for approximately 80% of total GSL isolated. Predominant gangliosides were N-acetylneuraminyl-galactosyl-glucosylceramide, N-acetylgalactosaminyl-N-acetylneuraminyl-galactosyl-glucosylceramide and galactosyl-N-acetylgalactosaminyl-N-acetylneuraminyl-galactosyl-glucosylceramide. Incorporation of labeled galactose into GSL was compared in mock-infected and herpes simplex virus type 1-infected BGM cells. Herpes simplex virus type 1 infection resulted in a 3- to 4-fold increase in galactose incorporation into glucosylceramide and a decrease in galactose incorporation into galactosyl-galactosyl-glucosylceramide and N-acetylgalactosaminyl-galactosyl-galactosyl-glucosylceramide. The virus-induced alteration in the GSL labeling pattern occurred early in infection, before the release of infectious virus, and was not prevented by the presence of cytosine arabinoside. Treatment of uninfected BGM cells with cycloheximide resulted in alterations in the GSL pattern which were similar to those observed in herpes simplex virus type 1-infected cells. An early virus function, e.g., inhibition of host cell protein synthesis, is probably responsible for the observed alterations of GSL metabolism. Experiments with a syncytium-producing strain of herpes simplex virus type 1, herpes simplex virus type 2 and pseudorabies virus indicated that other herpesviruses altered GSL metabolism in a manner similar to herpes simplex virus type 1.