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An intracellular interaction between a temperature-sensitive mutant and the original wild-type HVJ (Sendai virus) is responsible for the establishment and maintenance of HVJ persistent infection
http://hdl.handle.net/2297/29179
http://hdl.handle.net/2297/29179200a0e10-4a82-4f5b-b6db-1ca420aafd9d
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-SATO-H-459.pdf (3.0 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-05 | |||||
| タイトル | ||||||
| タイトル | An intracellular interaction between a temperature-sensitive mutant and the original wild-type HVJ (Sendai virus) is responsible for the establishment and maintenance of HVJ persistent infection | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Sato, Hiroshi
× Sato, Hiroshi× Ogura, Hisashi× Hatano, Motoichi |
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| 書誌情報 |
Journal of General Virology 巻 55, 号 2, p. 459-468, 発行日 1981-01-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0022-1317 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00698722 | |||||
| DOI | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.1099/0022-1317-55-2-459 | |||||
| 出版者 | ||||||
| 出版者 | Society for General Microbiology | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | In order to understand the selective survival of temperature-sensitive (ts) mutants in persistent infection by HVJ (Sendai virus), an intracellular interaction between a ts clone (HVJ cl. 14) isolated from HVJ carrier G2 cells and the original wild-type virus (HVJo) was studied. HVJ cl.14 differed from HVJo mainly in its ts property at 39°C, weak cytopathogenicity and faster electrophoretic mobility of P protein (P(77K)), but showed similar trypsin-activated growth to that of HVJo. When LLCMK2 cells were simultaneously infected with HVJo and HVJ cl.14 at 32°C, synthesis of HVJo-derived P protein (P(79K)) was inhibited with concomitant reduction of cytopathic effect (c.p.e.) and more dominant growth of HVJ cl.14 was observed. For the analysis of progeny viruses in these mixed infections, another mutant of HVJo designated HVJe which formed plaques activated only by elastase was isolated and employed instead of HVJo. At 39°C, HVJ cl.14 was rescued by coinfected HVJe at about 900- to 13000-fold over single infection. This recovery was also shown by sequential synthesis of HVJ cl. 14-derived P protein (P(77K)) following the earlier synthesis of HVJo-derived P polypeptide (P(79K)) in the mixed infection at 39°C. However, the u.v. inactivation of HVJe or HVJ cl. 14 resulted in a loss of their activity on rescue or on c.p.e., reduction, suggesting the necessity of protein synthesis by opposite viruses for these interactions. The mechanisms involved in the predominant growth of the ts mutant and concomitant reduction of c.p.e. seemed to provide a general explanation for the preferable persistence of the ts mutant in the HVJ carrier cells. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
