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首页> 外文期刊>Journal of Virology >Virus production by Abelson murine leukemia virus-transformed lymphoid cells.
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Virus production by Abelson murine leukemia virus-transformed lymphoid cells.

机译：Virus Makess由Abelson鼠白血病病毒转化的淋巴细胞。

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Cell lines obtained by in vitro transformation of bone marrow with Abelson murine leukemia virus (A-MuLV) can be divided into three classes: producers, releasing reverse transcriptase-containing particles and infectious virus; nonproducers, releasing no viral particles; and defective producers, the most common phenotype, releasing particulate reverse transcriptase in the absence of infectious virus. When such cell lines were analyzed 1 to 2 weeks after their isolation, however, all produced infectious virus. Because these cell lines were carried in culture, many ceased to release infectious virus but produced defective virions. One defective producer, SWR4, has been extensively studied. The particles it produces have the same density as that of virions of Moloney murine leukemia virus (M-MuLV). The particles contain no 35 to 70S RNA, as determined by analysis of [3H]uridine-labeled particles, and exhibit no endogenous reverse transcriptase activity. Although the reverse transcriptase enzyme is of normal size, the major structural protein of the defective virions has a molecular weight of 28,000 (p28), in contrast to the p30 of M-MuLV, and no viral glycoprotein was evident. The defective particles do not appear to arise either from the helper virus or from Abelson virus. An alteration of the protein of the helper virus is an unlikely source of p28 because particles produced by lymphoid cells transformed with another strain of M-MuLV as helper (M-MuLV-TB) contained p28 with an unaltered cleavage pattern, although M-MuLV-TB p30 differs from M-MuLV p30. The A-MuLV genome lacks the capacity to code for the reverse transcriptase virions. Clones of fibroblasts infected with A-MuLV only occasionally produce defective particles. The defective particles therefore probably arose from an endogenous virus that is preferentially expressed in the class of lymphoid cells transformed by A-MuLV. This interpretation implies that the majority of A-MuLV-transformed lymphoid cells completely lose expression of the helper virus genome.
机译：通过骨髓的体外转化与Abelson鼠白血病病毒（A-Mulv）的体外转化获得的细胞系可分为三类：生产者，释放含有逆转录酶的颗粒和传染性病毒;非脯化剂，没有病毒颗粒;和有缺陷的生产者，最常见的表型，在没有传染性病毒的情况下释放颗粒状逆转录酶。然而，当分离后1至2周分析这种细胞系，所有产生的传染病病毒。因为这些细胞系在培养中携带，因此许多人停止释放传染性病毒但产生缺陷的病毒粒子。广泛研究了一个有缺陷的生产者SWR4。它产生的颗粒具有与Moloney鼠白血病病毒（MULV）的病毒粒相同的密度。通过分析尿苷标记的颗粒的分析，颗粒含有No 35至70s的RNA，并且没有内源性逆转录酶活性。尽管逆转录酶酶具有正常尺寸，但缺陷病毒粒子的主要结构蛋白质的分子量为28,000（p28），与Mulv的P30相比，没有明显的病毒糖蛋白。缺陷的颗粒似乎没有从辅助病毒或来自阿贝森病毒产生的。辅助病毒的蛋白质的改变是P28的不太可能的来源，因为淋巴细胞产生的颗粒与另一种菌株的M-Mulv作为辅助（M-Mulv-TB）含有P28，但Mulv含有未改变的裂解图案。 -TB P30不同于MULV P30。 A-Mulv基因组缺乏对逆转录酶病毒群的代码的能力。用A-MULV感染的成纤维细胞的克隆仅偶尔产生缺陷的颗粒。因此，缺陷的颗粒可能从内源性病毒产生，其优先在由A-Mulv转化的淋巴细胞类别中表达。这种解释意味着大多数A-Mulv转化的淋巴细胞完全失去了辅助病毒基因组的表达。

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