Abstract
The infection of baby hamster kidney cells with Semliki Forest virus results in the inhibition of [Me3H]choline incorporation into 3‐sn‐phosphatidylcholine of the cytoplasmic membranes of intact cells. This inhibition was also observed in purified plasma membrane and endoplasmic reticulum. The major decrease of incorporation of label occurred between 4 and 6 h after infection.Microsomes from baby hamster kidney cells infected with Semliki Forest virus exhibit approximately a 50% decrease in total activity and a 40% decrease in specific activity of the enzyme CDP‐choline: 1,2‐diglyceride cholinephosphotransferase. This decrease in enzymatic activity occurred between 4 and 6 h post‐infection. When compared to mock‐infected cells, the enzymatic activity from infected cells had a similar apparent Km for CDP‐choline and a similar half‐maximal stimulation value for 1,2‐diacyl‐sn‐glycerol. Experiments with cycloheximide and actinomycin D suggest that viral inhibition of host protein and RNA synthesis would not account for the depressed cholinephosphotransferase activity. However, since cycloheximide stimulates the choline‐phosphotransferase activity of mock‐infected cells, the results of these experiments must be interpreted with caution. A freely diffusable inhibitor was not detected in the microsomes from infected cells.Infection of baby hamster kidney cells with a picornavirus (bovine enterovirus) did not inhibit or stimulate [Me3H]choline incorporation into 3‐sn‐phosphatidylcholine nor did it affect the activity of CDP‐choline : 1,2‐diglyceride cholinephosphotransferase.