ウイルス
Online ISSN : 1884-3433
Print ISSN : 0042-6857
ISSN-L : 0042-6857
11 巻, 6 号
選択された号の論文の5件中1~5を表示しています
  • II. T3感染菌の蛋白, 核酸合成について
    松原 謙一, 渡辺 格, 木方 行郎
    1961 年 11 巻 6 号 p. 361-366
    発行日: 1961年
    公開日: 2010/03/16
    ジャーナル フリー
    1. 合成培地中で全菌にT3を感染させ, その示す反応を生化学的に調べる方法を確定した. この条件ではファージは12分頃から菌体内で増殖を始める.
    2. T3ファージ抗原蛋白の増加の様子を時間的に調べたところ前者はファージ増殖開始後5分頃から, 後者は0分から直ちに合成が始まるが, それ以降は溶菌により蛋白合成が停止する迄両者が共存的に合成され続けた. 非ファージ抗原性蛋白はColiタイプ蛋白とデンプンゾーン電気泳動では区別がつかなかつた.
    3. T3感染菌の核酸合成をその速度, 代謝的安定性の面からみるとColiタイプだが, RNAの顆粒への分布, β-2-チエニルアラニンの阻害作用の受け方はファージ感染タイプであつた.
    4. これらのふるまいはT3感染菌の合成反応にもT3のsemitemplate性が反映していると考えて説明された.
    研究費の一部は文部省科学研究費によつた.
  • 第三報 T3のデオキシリボ核酸燐の起原と分布
    景山 真
    1961 年 11 巻 6 号 p. 367-373
    発行日: 1961年
    公開日: 2010/03/16
    ジャーナル フリー
    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.
  • 第8報 PR8株を経鼻噴霧感染した場合と経腹腔感染した場合とに於ける肺病変の差異の病理組織学的追求
    佐々木 雄一郎
    1961 年 11 巻 6 号 p. 373-385
    発行日: 1961年
    公開日: 2010/03/16
    ジャーナル フリー
    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.
  • 多村 憲, 岩永 光比子, 東 昇
    1961 年 11 巻 6 号 p. 386-393
    発行日: 1961年
    公開日: 2010/03/16
    ジャーナル フリー
    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.
  • 1961 年 11 巻 6 号 p. 396-402
    発行日: 1961年
    公開日: 2010/03/16
    ジャーナル フリー
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