Bell J G, Wyke J A, Macpherson I A
J Gen Virol. 1975 May;27(2):127-34. doi: 10.1099/0022-1317-27-2-127.
Cultures of chicken embryo fibroblasts infected with the temperature-sensitive transformation mutant of Rous sarcoma virus, tsLA24PR-A, were arrested between mitosis and S phase by exposure to serum-free medium at the non-permissive temperature (41degree C) for 2 days. On shifting to the permissive temperature (35degree C) the cells assumed a transformed morphology and increased uptake of [2minus 3H]-Deoxy-glucose. There was a concomitant increase in acid insoluble [3H]-thymidine. This suggests that the virus transforming function can cause stationary cells to enter their growth cycle. The level of release of infectious virus was shown to decrease on cell cycle arrest in serum-free medium and not to recover on a shift to 35 degrees, when cellular DNA synthesis and transformation was induced. Cultures rendered stationary in medium containing serum depleted of multiplication stimulating factor did not show this reduction in virus production.
用劳氏肉瘤病毒温度敏感转化突变体tsLA24PR-A感染鸡胚成纤维细胞，在非允许温度（41℃）下将其置于无血清培养基中2天，细胞在有丝分裂和S期之间停滞。当转移到允许温度（35℃）时，细胞呈现转化形态，[2-3H]-脱氧葡萄糖摄取增加。酸性不溶性[3H]-胸腺嘧啶核苷也随之增加。这表明病毒转化功能可使静止细胞进入生长周期。结果显示，在无血清培养基中细胞周期停滞时，感染性病毒的释放水平降低，当诱导细胞DNA合成和转化并转移到35℃时，病毒释放水平未恢复。在含有耗尽增殖刺激因子的血清的培养基中停滞的培养物未显示出病毒产生的这种减少。
