In this report, I have made clear that the susceptibility of mice to the mouse encephalomyelitis virus was markedly increased when mice were treated with effective dose of Cortisone. 1) Multiplication of the virus in the brain was promoted. 2) Appearance of dermal inflammatory reaction by turpentine oil was delayed but an obvious effect on the cellular reaction in the brain when the virus made a remarkable multiplication could not be observed and it was known, in general, that appearance of the cellular reaction was slow compared with the rate of multiplication of the virus. 3) Phagocytic function of subcutaneous tissue cell decreased. 4) Antibody formation decreased but the mechanism of promoting the multiplication of virus proceeded this, and gave no effect on the existing antibodies. 5) Anatomically the atrophy of spleen and whole lymph nodes was remarkable. 6) No direct change on blood sugar level was observed regardless of infection with the virus. No immediate remarkable effect on serum protein was observed, but the rise of globulin following the infection could not be confirmed among the mice treated with Cortisone.
Therefore, when the way of thinking about the susceptibility is divided into the following two, the receptibity and the vulnerability, effect of Cortisone which increases the susceptibility is to increase the receptibity which allows the multiplication of pathogenic microorganism and the vulnerability which rises the symptome, on the contrary, seems to be decreased.* The hypofunction of R. E. system following the atrophy of spleen is the subject to be thoroughly searched in explaining the function of Cortisone. It seems that there are still doubtful points to be explained in the relation of the susceptibility to virus and the meaning mentioned above. (These points will be reported later.)

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1. In order to investigate serologically the immunity following smallpox revaccination, titration of hemagglutinating, complement fixing, and neutralizing antibodies in sera before and after revaccination was done in 299 persons.
2. Hemagglutination inhibiting antibodies (H. I. A.) were scarecely detectable in the sera before revaccination. They appeared or began to increase 10 to 14 days after revaccination, reached their highest titres in two to four weeks thereafter, and then began to decrease and finally almost disappeared in about half an year. The maximum titres were much lower than those observed in smallpox patients.
3. Complement fixing antibodies (C. F. A.) were also hardly detectable before revaccination, but after revaccination they appeared earlier than H. I. A. Usually they were demonstrable as early as 7 days after revaccination. Thereafter they showed almost the same relations as H. I. A. A crude antigen prepared from chorioallantoic membranes of chick embryos infected with vaccinia virus was found to be most satisfactory for complement fixation test.
4. No definitive relation was found between neutralizing antibody level before revaccination and local reactions after revaccination. As generally accepted, an increase in circulating neutralizing antibodies was observed in cases with successful response. In “failed” cases, further observations would be necessary thereof.
5. H. I. A., C. F. A. and neutralizing antibodies appeared or increased in most of “taken” cases, but not in “failed” cases. This fact would indicate that immunity does not increase when revaccination fails to respond.
6. The observations made of serum antibody level before and after revaccination suggested that misjudges might be possible in the clinical diagnosis of the local reactions caused by smallpox revaccination. Epidemiologically it is a serious problem to check cases as successful which have actually acquired no sufficient immunity after revaccination. Therefore, serological examination is recommendable in the study of immunity in case of smallpox revaccination.

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Electrophoresis of chicken egg white was carried out by means of the Tiselius' apparatus (Type HT-A, Hitachi made) with barbituric buffer of pH 8.6 and ionic strength of 0.1, observations being made of the alterations of relative concentration of each fraction according to egg-species, incubation-period and inoculation of bouillon or vaccine-virus.
1. There were significant differences in each alteration of the fractions F, A₂, A₁+A₂ and C₁ in comparing the egg white of the White Leghorn with those of the Rhode Island Red and New Hampshire.
2. There were also significant differences in the alterations of each fraction in comparing the White Leghorn's egg white with those incubated for 5, 10, 12, 13 and 15 days. At an early stage of incubation, the alterations of the fraction A were especially recognized and at a later stage of incubation those of fraction C.
3. The 10 day-incubated White Leghorn's eggs were divided into two groups. Each egg of the first group was inoculated with 0.05cc of bouillon (pH 7.4) and each of the second group with the chorioallantoic membrane of vaccine-virus diluted to 10% with bouillon (pH 7.4). On the 2nd, 3rd and 5th day after the incubation-namely on the 12th, 13th and 15th day from the time of incubation-the fractions of both groups were compared. On the 5th day the increasing of the fraction G was recognized in both groups and on the 2nd and 3rd day the alteration of the fraction G showed that in the eggs inoculated with bouillon and vaccine-virus there was a dissimilarity in comparison to the time elapsed.

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During the period from late summer till early fall of 1953, an acute febrile illness characterized by headache, moderate pyrexia and paroxysmal pain at the costal margin, sporadically occured in Nanyo Town, Yamaguchi, Japan.
Two patients were admitted to the Nanyo Hospital. Case 1 was H. Yoshimitsu, 20yrs. female and Case 2 was F. Nakai, 37yrs. female.
The intraperitoneal inoculation to one-day-old mice with fecal suspension collected from these patients, resulted in getting the isolation of one strain (Yoshimitsu strain) of virus from Case 1.
The mice during the first 3 days of life are completely susceptible by intraperitoneal inoculation of 10% infected mouse muscle suspension (Table I) and such mice die in three or five days showing tremor, ataxia, marked dystrophy, sometimes spastic paralysis or convulsion (Fig. I).
The ID₅₀ of a pool of mouse muscle material from the first passage was 10^-7.4 and that of brain was 10^-6.8 by intraperitoneal route.
Histological examination of such animals as infected with peritoneal routes, showed focal myositis, acute necrotic pancreatitis and steatites, but lesions of the cerebrum were not observed.
These findings indicate that the virus belongs to Group B Coxsackie virus.
Then the cross-neutralisation tests were made to infant mice with 100 ID₅₀ of three strains of Coxsackie viruses (Yoshimitsu, Dalldorf's Group B Type 1 and 2 viruses) and its specific antisera. The results of the tests are illustrated in Table II, which shows Yoshimitsu strain is identical with Group B Type 1 (Conn.-5) virus.
Furthermore neutralisation tests were performed with the patient's paired sera and the strain of Coxsackie virus referred to above (Table III). These two patient's acute phase sera were obtained on October 4, 1953 and convalescent sera were drawn on January 22, 1954, about 4 months after an attack of their illnesses.
In case 1, neutralisation index of the acute phase sample was 100, and the convalescent one was larger than 1000. In second case, we failed to isolate virus from her stool, and could not demonstrate neutralizing antibody in acute phase serum, but a specimen of serum obtained on January 22, 1954, gave neutralisation index larger than 1000.
A rise in the titer of neutralizing antibodies in the patient's sera shows that this virus is of human origin and played an etiological role in their illnesses.

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Purified virus suspensions used for the ultracentrifugal analysis of vaccinia virus have been prepared by many investigators by the method of differential centrifugation. However, the high speed centrifugal forces employed by these workers were varied considerably.
In the present experiments it was found that the final purified virus suspensions were contaminated with a component of 1300 S, much smaller than the virus particles, when the preparations were spun at 12, 000 rpm for 30 min. of high speed centrifugal force in the No.40 rotor of the Spinco Ultracentrifuge, Model L.
It is expected that centrifugation at 6, 000 rpm (about 2, 400g) for 30 minutes in this head is just enough to sediment the virus particles. In this way the contaminated component was eliminated and the resulting virus suspension demonstrated a relatively well defined single boundary formed by the virus particles of about 5, 400 S.

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The distribution of hemagglutinin inhibitory antibody was investigated throughout the whole territory of Japan. It was revealed, that the antibody was detected in a more or less remarkable degree throughout whole Japan. Being compared with that against influenza virus, type A (PR8), however, the antibody against HVJ was detected in a considerably variable degree showing the fact, that the infection by this virus is not get coming to the final stage of the epidemic although it is able to be found throughout the whole territory of Japan.
A specially high antibody was found in the blood of the citizens of Sendai city, being compared with that of other district (Iwadeyama town) of Miyagi prefecture. This fact indicated that the virus prevails in the city of Sendai in more concentrated degree.

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In this communication a report is made on hemagglutination by dengue virus (Hawaiian strain).
The results are summarized as follows.
The conditions of hemagglutination reaction:
1. A specific hemagglutinin was recovered from 2 to 4 day-old mouse brain infected with the virus of dengue.
2. The virus material was made into a 20% suspension with 5% glucose solution (pH 6.8), and further it was diluted two-fold in 1.5% calcium chloride solution (pH 6.8) to obtain a 10% suspension. The suspension was centrifuged at 9, 600 r. p. m. (8, 500 G) for 10 minutes.
The supernatant fluid was employed as the virus material.
3. 0.25% or 0.3% suspension of horse red cells and 1.5% calcium chloride solution (pH 6.8) were used respectively as blood cells and reaction medium.
4. Optimal temperature for the reaction was 4°C.
It was recognized that under those conditions dengue virus agglutinated horse red blood cells as high as 81, 920 to 163, 840.
Specific properties of hemagglutination reaction
Hemagglutination reaction by dengue virus was inhibited by dengue hyperimmune mouse and rabbit sera, but not inhibited by normal mouse, normal rabbit, mouse encephalomyelitis (GD VII) hyperimmune rabbit, influenza (PR 8) hyperimmune rabbit, polio. patient and normal human sera.
Accordingly the hemagglutination by dengue virus is considered as specific. In addition, mouse and rabbit sera contain a nonspecific inhibitor for the dengue hemagglutinins. However, it was confirmed that specific hemagglutination-inhibition antibody was readily separated from the normal inhibitor above mentioned by extration with chloroform.

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Studies have been made of the effect of ectromelia virus upon the Ehrlich mouse ascites tumor. It was found that the virus multiplied in the tumor cells. In the course of this work the appearance of two types of cytoplasmic inclusion bodies were recognized as it was the case with monocytes. In smears the first type stained azurophilic (A-inclusion) and the other type pale bluish (B-inclusion). From the view-point of morphological criteria with aid of the histological observation and electron microscopy of ultrathin sectioning specimens made at various intervals after virus inoculation, the azurophilic inclusions, appearing in the early stage, appear to coincide with DNA positive matrices which are synthetized by infected cells themselves and contain some developmental viruses. At the next stage, the second type (B-inclusion) appeared in a close relation with the azurophilic inclusion. The latter was classified in about 4 types by their internal structures which varied from one extreme of superficial attachment of viruses to another extreme of internal filling with viruses. The author discussed the mechanism of ectromelia virus multiplication through the formation of inclusion within the Ehrlich ascites tumor cell.

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