In the microscopic studies on the rabbit cornea tissues infected with vaccinia virus, the following results were obtained.
1) Within the cytoplasm of the infected cells, matrix area and the so-called “inclusion bodies” were recognized.
2) Elementary particles could not be seen in the so-called “inclusion bodies”.
3) The matrix inclusion bodies are occupied by masses of viral particles, which appear to be at various developmental stages, and by fine granular substances.
4) It was observed that a part of the immature viral particles in the matrix inclusion bodies was composed of nucleoid and viroplasm and further that they were surrounded by membranes.

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Electron microscopic study was carried out on the ultrathin sections of the chicken embryo chorioallantoic membranes harvested at 4 days after inoculation of ectromelia virus. The results obtained are summarized as follows;
1) A large number of inclusions bodies and elementary bodies were observed in the cytoplasm, and the inclusions bodies, larger or smaller, so high in density and amorphus, that any elementary body was unable to be recognized in these bodies. These inclusions bodies, bowever, included groups of the mature viral particles, which were quadrat in form and 200-250mμ in size.
2) In the so-called matrix region higher in density, viral particles which are mature or at various stages of development were observed.

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Cultivation of Izumi-fever virus in tissue culture was attempted with various kinds of tissue, i.e., heart, lung and kidney of suckling mouse, rat, guinea pig, sand rat and human embryo, and chicke mbryonic skinmuscle and chorioallantoic membrane.
The cultivation of this virus was carried out through stational method in the medium consisting of Hanks' solution 60%, ultrafiltrate horse serum 30% and chick embryo extract 10%.
No cytopathogenic effects were observed in any case. Therefore, histopathological changes of rats sacrificed 30 days after inoculation with the culture fluid of the 3rd passage of tissue culture were investigated. The histopathological changes showed that this virus multiplied more favorably in heart and lung tissue than in kidney tissue throughout all species of animal used.
In developing hen's egg, yolk sac method and allantoic cavity method were used. In both cases, this virus failed to cause fetal infection, and no hemagglutination was observed. The histopathological changes of rats inoculated with egg material of serial passages, showed that yolk sac method was superior to allantoic cavity method to cultivate this virus.

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Many studies on HVJ such as the growth characteristics in eggs or in tissue culture flasks have been already reported from this laboratory. The present paper deals with the growth curves of this virus in mouse lung with particular emphasis on the comparison between mouse-passage and egg-passage strains, in respects of their pathogenicity, maximal growth estimated by infectivity for eggs or by hemagglutinin, and the changes of the amount of heat-stable inhibitor in mouse lung following infection with varying amount of inoculum.
Although both mouse-passage and egg-passage strains produced pulmonary lesions in young mice, following differences have been noted between them. First, the former was more virulent in inducing lesions in mice with comparable amount of inoculum. Second, the hemagglutinin titer at the peak of growth was higher with the former. Thirdly, the enzymatic activity destroying the inhibitor was stronger with the mouseadapted strain. However, the virus titer estimated by infectivity for eggs and the time length of its maintenance in mouse lung were recognized to be almost equal with both strains or rather higher with egg-passage strain.
In addition, facts have been presented which indicate that the appearace of hemagglutinin is accompanied with the reduction in the amount of heat stable inhibitor and the disappearance of the former is accompanned with the reappearance of the latter. The multiplication of the virus estimated by HA appeared to be closely correlated with all these couses of changes, while the virus titer assayed by egg infectivity did not speak too much with these changes. The lesions are usually induced at the time of disappearance of the inhibitor. However, these lesions proceed gradually up to develope the whole consolidation of the lung irrespective to the reappearance of the inhibitor. Therefore, the development of lesions seems to have uo correlation with the presence or absence of the inhibitor in the lung.

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The acetone-ether extracted brain antigen for complement fixation test of Izumi fever was prepared according to Casals' procedure. The SG strain was used for this purpose.
A preliminary examination was carried out with Casals' powder as antigen, but it showed only a low antigenicity and a high anticomplementary action.
Therefore, Casals' powder was extracted further with about 10 volumes of distilled water or saline 3 times in a mortor and the pooled extract was saturate with ammonium sulfate to 2/3. By this procedure a portion of anticomplementary activity was able to be removed into the supernate. The active precipitate was again dissolved in water, dialyzed against running water and precipitated again by ethanol. The precipitate thus obtained was dissolved in saline and used as a purified antigen. The ethanol precipitated antigen had no anticomplementary action, but had a high antigenicity.
The results of several experiments using this purified antigen were described. Beside immune sera from guinea pigs, serum from a human volunteer taken 3 weeks after the administration of etiological agent, and sera from Izumi fever patients taken 2-6 months after onset in the epidemic in Yamagata prefecture, possessed high C. F. antibodies. From these results, though the tested specimens were fairly few, the possibility of application of C. F. T. for practical diagnosis of Izumi fever was suggested.
In addition, the problems of the purification of C. F. T. antigen from infeted mouse brain, especially for the elimination of the anticomplementary substance, were discussed.

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It has been reported that the antigenic conversion from 3, 10 to 3, 15 in group E Salmonella is of a nature of lysogenic conversion and the phage responsible for the conversion is obtained from group E₂ and E₃ Salmonellas, and that the antigenic structure of variants is reverted to the original one by cultivating the cells in broth containing anti-15 serum.
This paper deals with the investigation on the relationship between the structure of O antigens and bacteriophage in lactose-fermenting organisms with the complete antigens of S. newington of group E₂.
Strains #2922 and 3534, which have been described by Saphra and Seligmann, were found to produce phages identical with the phage ε¹⁵ in the activity of inducing lysogenic conversion from 3, 10 to 3, 15 in the O antigens of group E Salmonella, plaque morphology, host range, serological specificity, etc. These strains split off lactose slowly fermenting or non-fermenting cells, which are not different from lactose fermenting cells in their lysogenicity. In addition, cells of antigenic structure 3, 10 were isolated when cells of antigenic structure 3, 15 were cultured in broth containing anti-15 serum, as observed in group E Salmonellas.
These strains are similar to Escherichia coil in that they ferment lactose and do not produce H₂S, but on the other hand they have been found by the author to be similar to Salmonella in the activities of amino acid decarboxylases. At the present stage of research, however, it is difficult to say to what extent either of the above properties is important to lysogenic conversion and production of the phage ε¹⁵, since, as will be reported in separate paper, among strains of Escherichia freundii with O antigens 3, 10 the similar lysogenic conversion of O antigens by the phage ε¹⁵ has been observed in a strain which is closely related to Salmonella in various biochemical activities including lactose fermentation but shows the activities of amino acid decarboxylases similar to those of Escherichia.

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No serological difference was noticed in neutralization test between or among different strains of phage which were obtained from S. newington, S. selandia, S. newbrunswick, S. cambridge and S. kinshasa of group E₂, and S. canoga, S. illinois and S. thomasville of group E₃.

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本論文においてはファージ感染菌における溶原化の 「決定」 と 「完成」 の問題が取扱われる.
増殖中の駒込BI菌 (Shigella flexneri, Variant Y) に菌あたり10以上のβファージを感染させると, 感染菌の約80パーセント以上が溶原化するのに対し, 菌あたり1-2個のβファージが感染した場合には溶原化率は僅か5-10パーセントにすぎなかった.
この現象は, 一見, 溶原化の成立がβファージ液中に含まれる少数の異質ファージ (高率で溶原化をおこすような) によつて決定されるという考え方を許容するが, この可能性は感染菌におけるファージの変態, 即ち前プロファージ状態を定量的に追究することによつて否定された. 即ち, βファージは溶原化に関して 「均質」 であつて, BI菌に感染した各ファージ粒子は相互に等しい確率 (0.07) で溶原化すると考えることによつて上の現象は説明された.
又, 溶原化の 「決定」 は時間的には感染後10分以内に完了するが, その後各ファージ粒子がプロファージ状態を 「完成」 する迄には, それらは非感染性且つ非増殖性の前プロファージ (Preprophage) として感染菌の子孫の間に7-11代もの間伝達されてゆくことが推定された.
こゝで, 一般にプロファージは宿主溶原菌の核機構と関連して存在すると老えられているのに対し, 溶原化過程の一段階である前プロファージ粒子は, 菌の分裂に伴つて全くat randomに子孫菌に分配される点で, 原形質内に自由な形で存在すると思われる事が注目された.

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This is a review of the literature on the etiology of epidemic keratoconjunctivitis (EKC). Adenovirus type 8 was first isolated by Jawetz and others from a case of EKC. They demonstrated that in majority of EKC cases, specific neutralization antibodies to this virus can be demonstrated while they are uncommon in normal controls. They also demonstrated that a striking rise of this antibibody occurs in the convalescent serum of this disease. The second strain of this virus was isolated by Chang in Saudi-Arabia from a probale infantile from of EKC, and the third strain by Mitsui and Jawetz in Kumamoto from a case of EKC. Five human volunteers were inoculated by Mitsui with the strain isolated by Jawetz. Four of the five showed a “take”. The findings were typical of EKC in three of the positive four and the findings in the last one were also not contradictory. In all of the four cases, there occured a striking rise in the specific neutralizing antibody to this virus, and re-isolation of the virus was succesful on two cases. In a fifth volunteer the inoculation was negative. A significant neutralizing antibody titer was demonstrated in the serum of this cases obtained before the inoculation. All of these results indicate that the etiological role of adenovirus type 8 in EKC is highly possible.

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