Abstract
Actinomycin D (AMD) pretreatment (0. 5 μg/ml, 72h) causes surface glycoprotein accumulation in 37 RC and Vero cells (submitted for publication). On the other hand glutamine starvation in these cells does not inhibit the cell replication but reduces the cell adhesiveness to the plastic and glass substrates probably by depletion of glucosamine pool. In such metabolic conditions the modifications of plasma membrane flexibility could be expected. Since such a flexibility influences Sendai virus maturation we decided to study the replication of this virus in AMD pretreated and glutamine starved cells.Three groups of 37 RC and Vero cells grown in monolayers, one untreated control, one AMD pretreated and one glutamine (G) starved were infected with Sendai virus. At 3. 5h and 24 h of infection corresponding cultures were fixed by: (a) classical methods, (b) TAPO techniqe and (c) ruthenium red method.
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