Influenza A (1953) and B (1954) isolated and propagated in human embryo tissue cultures differed from the same viruses passaged only in the chick embryo in regards to certain hemagglutination characteristics and other reactions with receptors. Thus, fowl erythrocytes were agglutinated at 4°C but not at 25°C by the TC line of influenza A and at either temperature by the E line. The former even when inactivated did not agglutinate sheep red blood cells, while the latter agglutinated these cells at 4°C but not at 25°C. Temperature dependence of the reaction with sheep erythrocytes was also demonstrated with the TC line of influenza B, and titers were lower than those with red blood cells from other species. The E line of this virus, in contrast, agglutinated sheep cells at either temperature and at relatively higher titers.Disagglutination of the virus-erythrocyte patterns occurred at a more rapid rate with the TC lines of influenza A and B than with the E line. This was observed at 5°, 25° and 37°C, with human, fowl, sheep and monkey erythrocytes, and with adsorbed-eluted virus as well as that contained in tissue culture or allantoic fluids. Patterns with human and fowl erythrocytes were maintained when inactivated virus was used except for the TC line of influenza A with fowl red blood cells.Elution rates of both TC viruses from human and fowl erythrocytes were more rapid than those of the E lines at 25 or 37°C. The TC line of influenza A was adsorbed poorly by fowl erythrocytes and not at all by sheep red blood cells. Both lines of influenza B were adsorbed more rapidly by fowl than human erythrocytes Degree of adsorption was correlated with hemagglutination behavior. The virus-erythrocyte combinations that agglutinated at 25°C showed more virus adsorption at 15–24°C, while those that required 4°C were adsorbed more rapidly at the same temperature. Amount of inactivated virus adsorbed increased progressively with temperatures between 5 and 37°C.More human urinary mucoprotein was required to inhibit hemagglutination by the TC lines of both viruses. Also, higher dilutions of normal rabbit serum inhibited the TC line of influenza A than the E line; slight differences in the opposite direction were found with influenza B. Differences between the virus lines in enzymatic activity as determined by receptor destruction were not demonstrable with human urinary mucoprotein, intact erythrocytes or their extracts.Both lines of influenza A behaved similarly in adapting to the mouse lung after serial passages. The E line, however, lost its adaptation to the allantoic sac and ability to agglutinate fowl cells at 25°C after mouse passages. The E line of influenza B adapted to the mouse lung after approximately the same number of passages as influenza A. The TC line, on the other hand, did not adapt even with 23 passages.
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