The inhibitory action of Gantrisin (a sulfonamide drug) of 0.2% concentration on the Virus T₆g and Escherichia coli F₆ system has been investigated.
When Gantrisin was added to this system within 8 min. from the time of infection and the concentration of the drug was maintained successively at 0.2%, neither lysis of this system nor the increase of active viruses were observed. But when the drug was removed from this system by dilution at adequate times before 8 min. after infecton, latent period and burst-size were observed in accord with the control one step growth experiment.
When this system in the presence of Gantrisin was diluted at adequate times over 9 min. after infection, latent period was prolonged in proportion to the interval between 8 min. and the time of dilution, but the burst-size remained the same as the normal one step growth experiment.
It is assumed that Gantrisin may attack some essential reactions relating to the synthesis of virus, and the synthesis process of virus is fixed by the action of Gantrisin at the state of 8 to 9 min. after infection as long as the drug exists successively.

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In the previous paper the authors reported on the isolation from the influenza-like disease of swine and the some properties of the virus. And, relationship between newly isolated virus and influenza virus of human type and NDV was reported. In this report, 17 young swines (weighing 8-10kg). 4 swines (weighing 18-22kg) and 3 swines (weighing 40-45kg) recieved by intraperitoneal, intravenous and intracerebral inoculation (as Table 1) 1ml of infected allantoic fluid (SEE strain was used), were observed as follows:
1. Clinically, some of swine developed a slight temperature, coughing, trembling, blear-eye, nasal discharge and diarrhoea, regardless of routes of inoculation and weighing. The many swines of weighing 8-10kg (i. n 6/8, i. v 3/3, i. p 2/3, i. c 3/3) were observed the stopping of growth and severe leaness. And the some of these swines (i. n 2/8, i. v 3/3, i. p 1/3, i. c 3/3) died. But, did not observed these symptoms in the all swines of above 18kg.
2. In haematological changes, the appearance of myelocyte, metamyelocyte and the slight increase of rod nuclearcells in neutrophiles were observed. Also, moderate increase of monocyte was observed. White blood corpuscles decreased to some extent in the some swine.
3. The virus was recovered at 7 and 17 days after inoculation from the lung and at 7, 17 and 52 days from the trachea by amniotic method.
4. Fig. 2 showed antibody response of young swine inoculated intranasally. H. I antibody achieved at 2 weeks after inoculation to maximum levels and lost already at 5 weeks. C. F. T antibody achieved at 4 weeks to maximum levels and lost at 6 weeks. Neutralizing antibody achieved at 2 weeks to maximum levels, but did not lose at 6 weeks.
5. Microscopically, 9 cases inoculated with this virus intranasally were investigated. In the lung of 8 case, the interalveolitis (which show the thickness of alveolar septum.), bronchiolitis and peribronchiolitis and in 1 died case and in the lung of all the cases inoculated intracerebrally, intraperitoneally and intravenously, congestion, haemorrhage and edema were observed. In other organ, the changes which based on circulatory disorder, atrophia of follicle (8/8) and haemorrhage of medullary cord of spleen (8/8), haemorrhage (7/8) and central necrobiosis of liver (3/8), haemorrhagic glomerulonephritis (4/8), interstitial nephritis (4/8), haemorrhage (6/8) and hyperplasia of reticulumcells of lymphnode, perivascular cuffing and hyperplasia of gliacells (1/9) were observed.

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The susceptibilities of several animals against the virus, which had been isolated from the influenza-like disease of swine, were examined.
Mice were infected by each route of inoculation such as intranasal, intraperitoneal, intracerebral and subcutaneous routes. The pulmonary consolidation was observed regardless of route of inoculation. The virus multiplied mainly at respiratory organ after inoculation by any route.
Mice inoculated intranasally showed clear symptom and all of them died between 5 to 7 days. Mice, the other hand, inoculated intraperitonealiy and subcutaneously did not showed any symptom, but virus multiplication and consolidation were observed in the lung. The mice inoculated intracerebrally showed the convulsive nervous symptom at 12-48 hrs. after inoculation. Seral passages by intranasal route with lung emulsion were successful within 11th passage and discontinued. Serial passages by intraperitoneal route with either lung and mixture of spleen, liver and lymphnode, were unsuccessful.
Young rabbit adult rat and hamster showed the considerable susceptibility. Rabbit and rat showed the mild symptoms which are similar to mice. Serial passages were successful within 6th passage by rabbit and 5th passage by rat, and discontinued. Hamster did not show any symptom, but serial passages were successful within 4th passge, and further passage failed. Guinea pig showed slight temperature rise and the virus was detected in the respiratory organ at 7th day after inoculation. But serial passages became negative at 3rd passage.
In 40 days old chick, the virus did not develop in any organs, but produced H. I antibody.
The fact that the resistance to infection remarkably developed in company with development of age of host, was observed in rabbit and mice. This fact coincided with the result of the case of swine described in the previous report.

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Recently, five lysogenic strains of Pseudomonas solanacearum E. F. SMITH were isolated by N. OKABE In the present study, one of them, strain T-c200, was used for virological and genetical investigations.
The lysogenicity of strain T-c200 is a stable hereditary character and its cell progeny consists wholly of lysogenic cells.
The virus, liberated from strain T-c200, is active against P. solanacearum strain S-9, S-Ix, E-3, A-8 and S (Table 1), and some of these indicator strains can be lysogenized.
During the logarithmic growth phase of strain T-c200 in potato-dextrose solution at 34 C, the increase of free virus is paralleled by the growth of bacteria, and the ratio of bacteria/free virus is constant, i.e. about 5×10⁴/1 (Fig. 1). It is assumed that the bacteria which spontaneously produce mature virus are a small fraction of the whole bacterial population.
Strain, T-c200 and its free virus are killed by irradiation with ultra violet light, and the ratios of inactivation of bacteria and virus are the logarithmic function of the irradiation dose (Fig. 3).
The proportion of strain T-c200 which produces mature virus is not increased but decreased by irradiation with ultra violet light (Fig. 3); therefore, strain T-c200 seems to be a non-inducible lysogenic strain.
After ultra violet light irradiation, bacteria without lysogenicity can be obtained from surviving colony formers. The bacteria, having lost their lysogen icity, are sensitive to their original virus but able to be relysogenized. Thus, lysogenic bacteria may be cured from their lysogenicity by ultra violet light irradiation. The loss of lysogenicity is never spontaneously reversed. Thus this bacterial character must have undergone a genetical change.
The mechanism of the loss of lysogenicity by irradiation with ultra violet light is discussed.

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The present paper deals with an ectromelia virus, which was isolated from liver of hybrid mice, during several attempts to obtain the causative agent of Izumi fever.
At first, blood specimen taken from a patient diagnosed as Izumi fever, was inoculated intraperitoneally to mice. Subsequent passages were performed 3 times successively, by intraperitoneal injection of resected liver. At the 4th transfer some characteristic changes of liver were noticed in all tested animals. But other viscera, such as lung or spleen were not so affected. Moreover the surface tinge of the liver was so similar to that of described as mouse hepatitis virus rather than that of ectromelia virus, so the picking of hepatitis virus latent in tested mice was anticipated. Subsequent transfers were performed further and fertile egg culture was also examined.
By the inoculation of mice liver suspensions into chorioallantoic cavity, CCA activity of fluids was proved.
Further the serological identification of the HA assured that the agent is NPV. NPV is an agent which is related to influenza viruses and was isolated in this laboratory in 1952 from the case of newborn pneumonitis. Afterwards the latency in mice was also ascertained in this laboratory. However the liver damage observed in this experiment was so conspicuous, so the reason of this liver changes deemed probably not owing to NPV.
So the contamination of both NPV and hepatitis virus was assumed and the separation of both virus was intended. Chicken cell adsorption of the chorioallantoic harvests at low temperature was repeated and the supernate was combined with anti-NPV rooster serum. After the above treatment, the supernate injection to mice, caused the death of mice representing the same characteristic changes of liver, But now, the further transfer in fertile eggs could not produce any HA. Thus the removing attempt of the NPV from this agent was successful.
But after the removing of the NPV, further examination proved that the virus is related rather to ectromelia virus than hepatitis virus. By foot pad inoculation, amputation of hind legs was occured. Spleen necrosis and presence of inclusion bodies in monocytes of ascites was ascertained by intraperitoneal injection. Pock formation on the chorioallantoic membrane became also evident. So the original virus was confirmed to be an ectromelia virus. Some characteristics of the virus were summarized as follows: LD 50 for mice weighing 12g in average was 10.^-8.5 Some decreases of titer were seen after filtration with Berkefeld N candle. The virus was precipitated by protamine sulfate.
The distribution of virus in several viscera after intraperitoneal injection was also determined and the high concentration was proved in liver, spleen and intestines. Other incculation procedures, such as intranasal instillation, also caused the death of mice, but prolongation of survival time was observed. Contrary to my expectation, histopathological changes and the virus distribution in each viscera by other inoculation routes was not different in principle from that observed by intraperitoneal inoculation, Young guinea pig was also susceptible against this virus.
Electronmicrographic studies were made in detail and the results were compared with that of standard ectromelia virus (Tama-strain). Though the same picture with standard virus was obtained after the treat ment with dil. sod. hydroxide, native picture was clearly different from each other.
From several results described above, the virus isolated thus in this laboratory from hybrid mice was assumed to be an ectromelia virus, although some differences in electronmicrographic figures were noticed.

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Between mouse brain (MB) and 12-day-old chick embryo body (CE) tissue, as materials for the preparation of JAPANESE ENCEPHALITIS vaccine, several differences were found:
1) Total Nitrogen content of MB tissue was 2.3 times while the supernate of MB centrifuged at 2500r.p.m. for 15 minutes contained 1.2 times as much Nitrogen, 2) total solids of MB was 2.6 times, 3) mouse intracerebral titers of infected MB tissue were from 6.3 to 200 times, 4) and calculated mouse i. c. LD 50 per mg Nitrogen of MB supernate was from 5, 4 to 170 times, all the above mentioned, approximately, as compared with those of CE tissue. 5) In the cross complement fixation tests using MB and CE antigens with the corresponding immune guinea pig sera, the reaction in homologous relation were stronger than in heterologous relation. 6) Any significant differences in neutralization indices could not be found in cross neutralization test using the same immune guinea pig sera as in c. f. test, and the corresponding both viruses. 7) In cross immunization tests in mice which were vaccinated with MB and CE vaccine and challenged with both viruses, the protection in homologous relation was not necessarily stronger than that in heterologous relation. 8) The protective power of CE vaccine was disproportionnally weaker than that of MB vaccine on the basis of infective titer before inactivation of vaccine. 9) The heated infected mouse brain suspension have a tendency of lowering LD50 titer when added to MB or CE virus in infectivity titration. The same was not observed in the heated CE suspension. This inhibiting effect on virus seems to be partly nonspecific.

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The causative virus of the rubella was found to be transmitted to children (Hiro and Tasaka, 1938) and to monkies after several passage on the chorioallantois of the chick embryo. Transmission test to mammalia except for human and monkey has not been successful until to-day.
The blood for inoculation were taken from two patients, who had been attacked with rubella on epidemics in Itabashi area of Tokyo in 1952 and 1953, and injected into testicles of guinea pig for the purpose of isolation of the causatve virus.
More or less than 7 days after the inoculation, there was a noticeable leucopenia and the relative lymphocytosis, though on the absolute numbers, the lymphocytes did not show any remarkable reduction, but neutrophile leucocytes.
Histo-pathologic findings of the inoculated animals, as follows: it showed the hypertrophy and hyperplasia of follicles, proliferation of reticulo-endothelial cells and sinus-catarrh in lymph nodes; septitis in lung; hypertrophy of lymph-follicles and proliferation of pulpa cells in spleen.
Fourteen volunteers recieved intracutan inoculation with emulsion of infected guinea pig testicles. One of them showed typical symptom of rubella, and 5 cases were diagnosed as abortive rubella without rush.

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