Mazur S, Feunteun J, de La Roche Saint André C
Laboratoire d'Oncologie Moléculaire, Centre National de la Recherche Scientifique, Institut Gustave Roussy, Villejuif, France.
J Virol. 1995 May;69(5):3059-66. doi: 10.1128/JVI.69.5.3059-3066.1995.
The state and expression of the hamster polyomavirus genome in a large panel of virus-induced lymphomas have been investigated. The viral genome is present within tumor cells either as abundant nonrandomly deleted extrachromosomal copies or as a single copy integrated into cellular DNA. We show that these two physical states are likely to be functionally equivalent: first, deletion and integration of the viral genome both inactivate the late coding region; second, the amount of viral early RNAs yielded by a single integrated copy appears to be very similar to that associated with several thousands of extrachromosomal copies of the viral genome. These data underline two essential requisites for hamster polyomavirus to become lymphomagenous: suppression of the late coding functions of the viral genome and expression of the viral oncogenes above a threshold level.
在大量由病毒诱导的淋巴瘤中，对仓鼠多瘤病毒基因组的状态和表达进行了研究。病毒基因组存在于肿瘤细胞中，要么是以大量非随机缺失的染色体外拷贝形式存在，要么是以整合到细胞DNA中的单拷贝形式存在。我们表明，这两种物理状态可能在功能上是等效的：第一，病毒基因组的缺失和整合都会使晚期编码区域失活；第二，单个整合拷贝产生的病毒早期RNA量似乎与与数千个病毒基因组染色体外拷贝相关的量非常相似。这些数据强调了仓鼠多瘤病毒成为淋巴瘤发生的两个基本条件：抑制病毒基因组的晚期编码功能以及病毒癌基因表达高于阈值水平。
