Abstract

Sendai virus grown in L cells (L Sendai) caused little hemolysis, whereas the one grown in fertile eggs (egg Sendai) induced distinct hemolysis. Enzymatic treatment with trypsin at low concentrations markedly enhanced the hemolytic activity of L Sendai but not that of egg Sendai. Both sonic treatment and freezing and thawing greatly enhanced the hemolytic activity of egg Sendai, but they gave little enhancing effect on that of L Sendai which could, however, be greatly increased by successive treatment with trypsin. Dose response and kinetic experiments on the trypsin effect have suggested that a similarity exists in the inhibitory mechanism of infectivity for L cells and hemolytic activity of L Sendai. Treatment of L cells with trypsin at later stages of infection released a highly hemolytic L Sendai from those cells. The present study, by reference to the density centrifugation studies in a previous report (4), has shown that a variation in infectivity for L cells and in the hemolytic activity of L Sendai is a type of host-controlled modification distinguishable from the density variation.

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