A method was described for infecting E. coli with T₃ in a synthetic medium for the study of biochemical behavior of T₃-infected cells. Under the condition studied, T₃ phage began intracellular growth at about 12 minutes. Synthesis of T₃-antigenic protein started at about 5 minutes after initiation of reaction, preceded by synthesis of non-phage antigenic protein with coli protein-like character. Synthesis of this non-phage antigenic protein did not sease even in the late stage of phage growth, but continued in parallel with synthesis of phage antigenic protein until cell sysis broke the protein synthesizing mechanisms.
Synthesis of nucleic acids in T₃-infected cells were compared to those of T₂-infected cells (which carry out phage-infected type synthesis), and uninfected cells (coli type synthesis). In T₃-infected cells, rate of increase of nucleic acids and metabolic stability of synthesized RNA were found to be coli type, while distribution of early RNA in cell constituents or susceptibility to β-2-thyenylalanine of RNA synthesis in T₃-infected cells were found to be phage-infected type.
These observations were discussed with consideration of T₃ phage which possess semitemplate character.

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1. The origin of phosphorous in T₃ DNA was studied. From three types of P³²-labeling experiments, whole labeling, host labeling, and medium-labeling, it was concluded that 84% of the phosphorous of T₃ derived from host cells, 16% from the medium after infection and 0.5% from parental phages.
2. The distribution of phosphorous of different origins among phage DNA were studied with ECTEOLA-cellulose column chromatography. The ratio, P³² content to optical density at 260mμ, was compared among chromatograms of whole labeled, the hostlabeled, and the medium-labeled T₃ DNA. There was no essential difference between them. So, it was concluded that phosphorous of any origin was distributed homogeniously among DNA molecules.

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Histopathological studies were made on mouse lung infected with the PR 8 virus intraperitoneally in an effort to differentiate the mode of infection from that of natural or intranasal infection.
First of all, the fact was noticed that the necrotic change or desquamation of the bronchial epithel, usually described as a characteristic feature of influenzal infections were not obvious when the virus was given intraperitoneally. However, the virus titers found with both lung tissue and bronchial washings were quite high and just comparable to the value obtained at the time of intranasal infection.
In order to explain the inconformities between the virus growth and development of consolidations described above, detailed study was carried out. Firstly, growth of virus, development of lung lesions and their correlations were carefully pursued against time. Secondaly, methylgreen and pyronine staining was used to examine lung tissues in addition to hematoxylin-eosin staining. As a result, it was found that the virus growth at the time of intraperitoneal infection was immediately accompanied by increased pyronine staining of bronchial epithel cell. This was concordant to the detected virus growth. In spite of this result, the necrosis or desquamation of these epithelial cell did not follow. Rather the development of consolidation, i.e. increase of histiocytes in alveorar septa was an event to be considered as a primary response.
The observation here made will point out the neccessity of plausible explanation for the desquamation of bronchial epithel which is usually found at the time of intranasal infections, but it was left for further studies. As a whole, the development of consolidation was understood as an immediate inflammatory response to the process of viral synthesis in bronchial epithel.

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As part of a general investigation of meningopneumonitis virus (MPV) multiplication in L cell, the nucleic acid content of the cells has been studied by direct chemical analysis at successive stage in the growth cycle.
Cal 10 strain of MPV and L cell suspension culture were used. Measurements of virus adsorption rate, distribution of MPV after adsorption and infective center formation indicated that essentially all cells were infected within 1 hour after addition of virus at multiplicity more than 50 PFU per cell.
Growth curves of MPV showed that an increase in intracellular virus began at 18.5 hours after infection and reached levels of 450-500 PFU per infected cell. It should be noted that the amount of intracellular virus titer during lag period dropped extremely below that number of infected cells, showing as low as 10^-3 PFU per infected cell at the lowest point.
In the experiments on the multiplication of infected cells, uninfected control cells multiplied until 25 hours, followed by stationary phase. But infected cell cultures did not show increase in cell number. Infected dead cells which were determined by staining with trypan blue were observed 20 hours after infection and almost all cells were dead within 35 hours after infection.
Nitrogen content in uninfected cells was constant until 40 hours, but in infected cultures decline was observed subsequent after 25 hours of infection. Protein content was constant until 20 hours, followed by dropping down both in infected and uninfected cells.
On the other hand, in analysing RNA and DNA contents per 10⁶ cells, although they were constant during 40 hours in control cultures, significant increase was observed in infected cells. The RNA and DNA increment in infected cells was first detected after 10 and 15 hours of infection, respectively, which proceeded an increase of cell associated virus by 8.5 and 3.5 hours. RNA content reached maximum at 20 hours after infection, followed rapidly decreased. DNA content continued to increase and reached near maximum approximately 25 hours after infection. Maximum increment of RNA and DNA reached levels about 133% and 135% of control cells, respectively.
From the results described above, it appears that both RNA and DNA are synthesized in MPV infected L cells. These polymer increment is demonstrable several hours before a significant increase in intracellular virus is found. The relationship of these increased nucleic acids to virus multiplication has been discussed.

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