It has been known for several years that a number of neurotropic viruses cause hemagglutination of erythrocytes
(1)-(13), and moreover, that varying the various conditions of hemagglutination, the spectrum of virus hemagglutination has been widely spread. Rheims et al
(14) reported that trypsin-trseated human group O red cells increased their agglutinability by mouse lung infected with PR 8 influenza virus, and Morris
(15) investigated that mouse encephalomyelitis virus (GDVII strain) agglutinated well human group O erythrocytes at 20 C in the presence of trypsin. In this laboratory also were obtained the similar results to those of Morris with trypsin and the following conclusions were reached that the mechanism of hemagglutination enhancement by trypsin seemed to be attributed to the increase of agglutinability of trypsin-treated red cells under a small amount of viruses, and on the other hand, to the digestion of hemagglutination inhibitors contained in mouse brain by the enzyme
(16).The present paper deals with enhancement of virus hemagglutination by the treatment of red cells with ficin, an intracellular plant protease, and by the treatment of virus suspension with the same enzyme.
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