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J Virol. 1970 November; 6(5): 637-643
Copyright © 1970 American Society for Microbiology. All Rights Reserved.

Phospholipid Synthesis in Sindbis Virus-Infected Cells

Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire 03755

ABSTRACT

We investigated the metabolic requirements for the decrease in phospholipid synthesis previously observed by Pfefferkorn and Hunter in primary cultures of chick embryo fibroblasts infected with Sindbis virus. The incorporation of ³²PO₄ into all classes of phospholipids was found to decline at the same rate and to the same extent; thus, incorporation of ¹⁴C-choline into acid-precipitable form provided a convenient measure of phospholipid synthesis that was used in subsequent experiments. Experiments with temperature-sensitive mutants suggested that some viral ribonucleic acid (RNA) synthesis was essential for the inhibition of choline incorporation, but that functional viral structural proteins were not required. The reduction in phospholipid synthesis was probably a secondary effect of infection resulting from viral inhibition of the cellular RNA and protein synthesis. All three inhibitory effects required about the same amount of viral RNA synthesis; the inhibition of host RNA and protein synthesis began sooner than the decline in phospholipid synthesis; and both actinomycin D and cycloheximide inhibited ¹⁴C-choline incorporation in uninfected cells. In contrast, incorporation of ¹⁴C-choline into BHK-21 cells was not decreased by 10 hr of exposure to actinomycin D and declined only slowly after cycloheximide treatment. Growth of Sindbis virus in BHK cells did not cause the marked stimulation of phospholipid synthesis seen in picornavirus infections of other mammalian cells; however, inhibition was seen only late in infection.