Abstract
In the past, all strains of Japanese B encephalitis (JBE) virus were thought to be antigenically the same. In 1954, Dr. Hale, however, described that the strains isolated in Malaya were not all the same but some antigenical differences were recognized among them. It was also suggested by Dr. Ogata that the antigenicities of the two Japanese strains, Nakayama and G-1, were found to be different from each other on the basis of cross-challenge test in mice, the former being isolated in 1936 and the latter in 1949. In order to determine whether or not the immunological differences might exist between those two strains, attempt was made to compare each other antigenically by means of cross-challenge test in mice checked weekly after the immunization on one hand, and on the other hand, by means of hemagglutination inhibition (HI)-, complement fixation (CF)-and neutralization-tests on pooled sera weekly collected from mice immunized with either virus. As a result, the mice immunized with Nakayama gave much higher resistance against challenge with the homologous strain than the heterologous G-1 strain within 4 weeks after immunization and the same trend, though it was slight, was observed in immunized mice following challenge with homologous or heterologous strain. Such antigenical differences were found, to some extent, between both strains by HI-, CF- and neutralization-tests on sera collected weekly from the immunized mice. As they did not give so clear cut result as the cross-challenge test, in the next study, sera taken from guinea pigs on every 2 days within 2 weeks after intracerebral inoculation with Nakayama or G-1 strain were examined for strain specificity. Sera taken on as early as 5 days after infection were found to have only strain specific antibodies.
Such phenomena as mentioned above were not caused by contamination of the strain with the other viruses sometimes encountered in a colony of mice, because both strains used were proven to be sensitive to desoxycholate and not to be precipitated by protamine sulphate. Furthermore, the antigenic structures of both G-1 antigens prepared front infected mouse brain at the 7th and the 196th passages were found to be almost the same.
This fact strongly suggested that G-1 strain antigenically different from Nakayama might not be a laboratory product during many passages from brain to brain, but could exist in situ in nature.
