Stanners C P, Francoeur A M, Lam T
Cell. 1977 Jun;11(2):273-81. doi: 10.1016/0092-8674(77)90044-7.
T1026, a ts mutant of VSV which is much less cytopathogenic than its parent, HR, and which can establish persistent infection under certain conditions, is a double mutant. In addition to its ts mutation in the virion RNA polymerase, T1026 has a second non-ts mutation in a viral function termed "P". This function is responsible for the inhibition of total protein synthesis in infected cells and acts chiefly at the level of translational initiation. In some cell systems, the inhibition of protein synthesis produced by P appears to be selective for cellular protein synthesis, whereas in other cell systems, both cellular and viral protein synthesis are inhibited. T1026 and its ts revertants are phenotypically P- -that is, cells infected with them show total protein synthesis rates equal to or greater than uninfected cells, while synthesizing viral proteins at the same or even greater rates than HR-infected cells. The P- mutation is correlated with failure to increase plaque size after 2-3 days of incubation. Since viral mutants obtained from persistently infected cultures in a variety of systems appear to be double mutants with a ts mutation in the virion RNA polymerase and a small plaque marker, we suggest that T1026 could represent a model for such mutants.
T1026是水泡性口炎病毒（VSV）的一个温度敏感（ts）突变体，其细胞致病性远低于亲本HR，并且在某些条件下能够建立持续感染，它是一个双突变体。除了在病毒粒子RNA聚合酶中存在ts突变外，T1026在一种称为“P”的病毒功能中还有第二个非ts突变。该功能负责抑制受感染细胞中的总蛋白质合成，主要作用于翻译起始水平。在一些细胞系统中，P产生的蛋白质合成抑制似乎对细胞蛋白质合成具有选择性，而在其他细胞系统中，细胞和病毒蛋白质合成均受到抑制。T1026及其ts回复突变体在表型上是P- ，也就是说，感染它们的细胞显示出的总蛋白质合成速率等于或高于未感染细胞，同时合成病毒蛋白质的速率与感染HR的细胞相同甚至更高。P- 突变与孵育2-3天后噬斑大小未能增加相关。由于从多种系统中持续感染培养物获得的病毒突变体似乎是双突变体，在病毒粒子RNA聚合酶中存在ts突变和小噬斑标记，我们认为T1026可能代表此类突变体的一个模型。
