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首页> 美国卫生研究院文献>Journal of Virology >Mutant of B-tropic murine leukemia virus synthesizing an altered polymerase molecule.
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Mutant of B-tropic murine leukemia virus synthesizing an altered polymerase molecule.

机译：B型鼠白血病病毒的突变体可合成改变的聚合酶分子。

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摘要

A nonconditional mutant of B-tropic murine leukemia virus (MuLV), defective in polymerase, has been isolated by cloning chronically infected cells. The cell clone containing the mutant produced virus particles which were noninfectious. However, superinfection of the cells by replication-competent XC-negative viruses resulted in the rescue of virus capable of forming plaques in a modified XC test, termed the "complementation plaque assay" (A. Rein and R. H. Bassin, J. Virol. 28:656-660, 1978). Analysis of the noninfectious virions produced without superinfection demonstrated that they contained only 2 to 5% of the wild-type level of reverse transcriptase activity. Purification of this activity indicated that it was associated with a smaller molecule than that produced by wild-type virus. Cells producing the mutant virions did not contain the gag-pol precursor, Pr180gag-pol; however the cells contained proteins of 147K and 114K daltons precipitable with anti-pol serum. All of the normal structural proteins as well as 70S genomic RNA could be detected in the mutant particles. An interference test indicated that a functional ecotropic glycoprotein was synthesized by the mutant. These results indicate that the mutant has a unique defect in the pol gene.
机译：通过克隆慢性感染的细胞，已分离出聚合酶缺陷的B-tropic鼠白血病病毒（MuLV）的无条件突变体。含有突变体的细胞克隆产生了非感染性的病毒颗粒。但是，具有复制能力的XC阴性病毒对细胞的过度感染导致能够在改良的XC测试中拯救能够形成噬斑的病毒，这种病毒称为“互补噬菌斑测定”（A. Rein和RH Bassin，J. Virol。28 ：656-660，1978）。对未进行超感染而产生的非感染性病毒粒子的分析表明，它们仅包含野生型水平的逆转录酶活性的2％至5％。对该活性的纯化表明，它与一个比野生型病毒产生的分子小的分子有关。产生突变体病毒体的细胞不包含gag-pol前体Pr180gag-pol；然而，细胞中含有147K和114K道尔顿的蛋白质，可通过抗pol血清沉淀。在突变颗粒中可以检测到所有正常的结构蛋白以及70S基因组RNA。干扰试验表明该突变体合成了功能性嗜糖蛋白。这些结果表明该突变体在pol基因中具有独特的缺陷。

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