(1) 萎縮病感染稲及び保毒媒介虫ツマグロヨコバイは燐酸代謝に異常を表わす. 本報告はこの異常現象に検討を加えるために, P³²を利用して観察した結果の一部を取纒めたものである.
(2) 稲, ツマグロヨコバイ共に燐酸各劃分に於けるP³²のturnover rateは, 罹病や保毒により低下する.
(3) RNAに於けるP³²のincorporationは, 稲, 媒介虫共にウイルスの影響をうけても, autoradiogramでのspotは数, 位置には差異がみられない. 尤もこのspotには紫外線吸収は認め難い. しかしてradioactivityは稲では罹患しても変化は少いが, 媒介虫では保毒により一般に強くなる.
DNAでのP³²のincorporationは, 稲, 媒介虫共に感染や保毒によつてもautoradiogramのspotには差異はない. 尚このspotには紫外線の吸収が認められる. しかしてこのradioactivityは感染保毒に伴つて著しく増強される.
(4) 稲及びツマグロヨコバイの酸溶性燐酸化合物は, LePage & Umbreit法によつて分劃観察した. Ba可溶及びBa不溶劃分は, 稲・媒介虫共に, ウイルスの影響によつてもP³²のincorporationに著しい差異はみられない. 又P³²のBaアルコール可溶分劃へのincorporationは, 稲・媒介虫共に極めて微量であり健病間に差異はない.

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(1) 媒介虫は保毒に伴つてもTCA-Cycle中のピルビン酸, クエン酸量には健虫に比べ差ががないが, コハク酸量は減少する. これは保毒中の呼吸衰退の一原因をなすと考える.
(2) 萎縮葉では還元糖, 水溶性糖は増加し, 不溶性糖と全糖は減少するが, 保毒虫ではいずれの糖も増加する. 即ちウイルスの感染保毒に伴い, 寄主・媒介虫に炭水化物の異常代謝が出現したと考えられる.
(3) 萎縮葉, 保毒虫共に健全個体に比べて可溶性窒素は増量し, 蛋白態窒素は減量する. しかして全窒素は両者とも減少する. これは感染保毒に伴い窒素代謝に変調が表われることを暗示している.
(4) 温州柑葉では遊離アミノ酸として, シスチン他14種, 媒介虫ではアスパラギン酸他12種がが認められるが, 感染保毒に伴う健病間の差異はない. 蛋白質構成アミノ酸は, 媒介虫では保毒によつても差異がないが, 寄主では感染によつてアラニン類似物質の新生を認める.
以上の結果より温州柑萎縮病ウイルスに感染保毒した寄主並に媒介虫は有機酸及び窒素, 炭水化物各代謝に変調を来たし, これらは呼吸, 燐酸, 核酸各代謝とあいまつて, それぞれの生体代謝に不均衡を生じ, 生体構成物質の動的平衡が破壊されて生活力に異常が表われると思われる.

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Salmonella anatum was lysogenized with a converting phage ε¹⁵. The resulting S. anatum (ε¹⁵) was infected with another converting phage ε³⁴ (m.o.i.=2.5), and the pattern of segregation of non-ε³⁴-carrying progenies from ε³⁴-infected cells was analyzed both by mass cultures and by single clone experiments. Both presented evidences that non-ε³⁴-carrying progeny cells were segregated out from ε³⁴-infected cells, but the segregation was to only a slight extent, suggesting that the phage ε³⁴ becomes an established prophage more easily and more quickly than the phage ε¹⁵.

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When S. anatum (ε¹⁵) was infected with temperate phage ε³⁴ or even with its virulent mutants, O antigen 34 appeared on the infected cells within 30 minutes. It indicates that the formation of the new character, antigen 34, was carried out even in cells which are destined to lysis. The mutation from temperate to virulent proved not to be related to the mutation in converting abilities.

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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.

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In the course of the studies on the i mutation of polioviruses it was found unexpectedly that mutants of poliovirus, forming minute plaque-m mutants were selected in some series of the serial passages of type 2 poliovirus (MEF-1) in tissue culture. Similarly m mutant of type 3 poliovirus (Saukett) was also obtained.
Selection of m mutants occurred usually in the course of several passages in tissue culture, but the factor or factors responsible for the selection of the m mutants remained undetermined.
The plaque size of m mutants was less than 0.5mm in diameter in HeLa, FL and monkey kidney cell monolayers, and certain factors such as PH and amount of agar overlay did not influence the plaque size.
m mutants were neutralized specifically by antiserum prepared against the respective m⁺ wild type viruses.
No apparent differences in both the cytopathogenic effect and the pattern of growth were observed between m⁺ and m mutants.
m mutants, after being purified repeatedly by limiting dilution technique, were proven to be stable through rapid serial passages in tissue cultures or mice.
m mutants of type 2 poliovirus were virulent for mice but a few of them were found to be less virulent than the wild type m⁺ virus.
m mutant, isolated after serial passages in tissue culture with inhibitory normal bovine serum, was found to have i character as well as the back mutant m⁺ i, obtained from the m i mutant. Furthermore i m mutant was obtained from i⁺ m mutant through serial passages in tissue culture with medium containing inhibitory bovine serum. Therefore it may be concluded that i and m mutation can occur independently from each other.

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1. Non-mouse-adapted vaccinia can produce the specific complement fixing antigen, but not mature virus in the Ehrlich Ascites tumor cells.
2. IHD strain of vaccinia produces the cytoplasmic inclusion body, the C.F.A. and mature virus in the cells.
3. In this system, the viral antibody can supress the inclusion body and C.F.A. formation.

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1) リフトバレー熱ウイルスをウサギ抗血清に加え, 約60,000g, 60分間遠心して得られた上清の中和力価はもとの血清のそれよりも低かつた. すなわち, 試験管内でウイルスを以て中和抗体を吸収することができた.
2) ウイルスと, それを中和するのに充分な量の抗血清とを混合し直ちに稀釈するとウイルスの一部分は活性を示すが, ウイルスの90%以上は不活性となつていた. 混合液を5℃に24時間おいた後に稀釈するとウイルスの99%が不活性となつていた.
3) ウイルスと抗血清とを混合し, 直ちにマウス脳内に注射すると明瞭には中和が起こらないものを5℃に24時間おいてから注射すると中和が起こつた.
4) 以上の諸成績から, リフトバレー熱ウイルスと中和抗体とは試験管内で結合すると考えられる.

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Multiplication of Cal 10 strain of meningopneumonitis virus (MPV) in vitro was studied using strain L cells as host cells. Relationships could be established among the developmental cycle of virus determined by infectivity titrations, the viral alterations within the cells tinctorially with light microscope, and the submicroscopical structures of various developmental forms and intracellular components, containing matrix, associated with virus under the electron microscopy.
It was found that a sharp decrease in infectivity titer of cell-associated virus during the first 18-20 hours was followed by an increase in titer 22-23 hours after infection, and then a few hours leter, free virus began to increase.
The yield of MPV in a L cell, estimated from the maximum titer of free virus to the number of infected cells, was about 600 mouse LD₅₀ per cell.
It was showed with Macchiavello's stain that hundreds of red stained particles (identified the elementary bodies at the terminal stage of development) were adsorbed on the cells soaked in a suspension of MPV for 2 hours, and a few hours later, most of these particles invaded to form a group in the central region of cytoplasm, where one or more blue stained large particles (initial bodies began to develop 8 hours after infection.
Some particles with elementary body-like structures attached to the cell membrane soaked for 2 hours and several similar particles in the cytoplasm (5 hours after infection) were photographed using ultra-thin sectioning. Single large body enclosed by a intracytoplasmic vacuolar structure (tinctorially invisible matrix) were the first appearance of developmental form of MPV, observed with the electron microscope.
Large bodies in the inclusion (20 hours) often presented a morula-like appearance showing their increase in number by segmentation. A number of elementary bodies (intermingled with various developmental forms) were observed in the inclusion at the initial stage of increase in titer (24 hours after infection).
And it was found that the titration of MPV in strain L cell based on the cyto pathogenic effect was not only sensitive and reliable but also available with ease.

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