Base mutations in the terminal noncoding regions of the genome of vesicular stomatitis virus isolated from persistent infections of L cells.
Base mutations in the terminal noncoding regions of the genome of vesicular stomatitis virus isolated from persistent infections of L cells.
复制标题
从 L 细胞持续感染中分离出的水疱性口炎病毒基因组末端非编码区的碱基突变。
DOI：
10.1016/0042-6822(85)90363-0
复制
发表时间：
1985
期刊：
影响因子：
3.7
通讯作者：
Keene,JD
中科院分区：
文献类型：
--
作者：
Wilusz,J;Youngner,JS;Keene,JD
The 3′-terminal regions of the genomes of vesicular stomatitis virus obtained from two long-term, independently initiated persistent infections of L cells were found to contain several sequence mutations. In contrast to the hypermutability displayed in the 5′-terminal regions of the genomes of viruses obtained from persistent infections of baby hamster kidney (BHK) cells (P. J. O'Hara, F. M. Horodyski, S. T. Nichol, and J. J. Holland,J. Virol.49, 793–798, 1984), no 5′ mutations were detected in viruses from L-cell carrier lines. The absence of detectable defective interfering (DI) particles in the L-cell carrier cultures may account for this difference. Plus-strand leader RNA made by the viruses from persistently infected L cells failed to accumulate from 5 to 8 hr postinfection unlike the accumulation noted for the leader RNA generated by wild-type VSV. Minus-strand leader RNA, on the other hand, accumulated at a similar or increased rate compared to wild type. The relationship of these observations to the processes of host shutoff, viral transcription, and replication are discussed.
