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The labeled lipid composition of Sendai virus grown in chick embryo (CE), cynomolgus monkey kidney (MR) and bovine kidney (BK) cells differed from that of these host ceils. In 20 hr labeling after infection with 32P‐orthophosphate, 14C‐acetate or 14C‐palmitic acid, virions had a high content of labeled phosphatidylethanolamine (PE) and a lower content of phosphatidylcholine (PC), while the host cells showed a reverse result. Virions also had a higher proportion of sphingomyelin than the host cells. Similar phospholipid patterns were also obtained by infecting cells labeled with 32P‐orthophosphate prior to infection. CE and MK cells labeled with 32P‐orthophosphate before infection followed by a 20‐hr labeling with 3H‐acetate revealed that lipids containing fatty acids newly synthesized after infection were incorporated preferentially into virions. The cause of these differences in lipid composition between the virion and the host cell should be sought. Relevant to this question was the finding that Sendai virus infection enhances not only total phospholipid synthesis, but also the PE and PC synthesis and presumably the pathway from phosphatidylserine to PE. These metabolic changes induced by infection may affect the lipid composition of the plasma membrane, hence that of the viral envelope.
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Hirano et al. (1971) studied this question.
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