Abstract
Sendai virus-induced hemolysis was markedly inhibited when human erythrocytes (RBC) were incubated with Sendai virus in the presence of concanavalin A (Con A). Pretreatment of RBC or Sendai virion with Con A was also found to lead to the inhibition of hemolysis, but the inhibition in these two cases did not appear to be of sufficient magnitude to account for the inhibition of hemolysis which occurred when RBC were incubated with the virion in the presence of Con A. On the other hand, the concentration of Con A inhibiting the hemolyzing capacity of the RBC-virion complex was close to that observed under conditions where Con A and the virion were added simultaneously to RBC. The effect of Con A was enhanced by treating the RBC-Con A complex or virion-Con A complex with anti-Con A antiserum, but the effect of Con A on the RBC-virion complex was slightly reversed by the addition of the antiserum. Divalent succinyl Con A had reduced ability to inhibit the hemolysis. The process of hemoglobin release was not affected by Con A. These results indicate that the inhibition is primarily the result of the crosslinking of Con A receptors in the RBC-virion complex.
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