Genetic structure of avian acute leukemia viruses.
Genetic structure of avian acute leukemia viruses.
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禽急性白血病病毒的遗传结构。
DOI：
10.1101/sqb.1980.044.01.086
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
Duesberg,PH
中科院分区：
文献类型：
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作者：
Bister,K;Duesberg,PH
根据其致瘤特性，禽RNA肿瘤病毒可分为几类：(1)引起动物结缔组织实体瘤的肉瘤病毒；(2)急性白血病病毒，引起快速造血功能紊乱和恶性肿瘤，以及肾和肝肿瘤，包括癌；(3)淋巴白血病病毒，通常在潜伏期很长后才引起淋巴白血病（Purchase and Burmester 1972; Hanafusa 1977; Duesberg，本卷）。然而，在体内和体外，这类病毒的致癌谱之间有广泛的重叠。在组织培养中，肉瘤病毒和急性白血病病毒都能转化成纤维细胞，一些急性白血病病毒在动物中引起肉瘤，而肉瘤病毒偶尔会诱导红母细胞白血病（Purchase and Burmester 1972）。RNA肿瘤病毒的转化被认为是一类被称为onc基因的独特基因的结果（Baltimore 1975）。劳斯肉瘤病毒（RSV）的一个基因被命名为src (Wang et al. 1976a)，以解释RSV诱导的主要肿瘤形式。src基因的定义和表征已经实现了使用遗传以及生化程序。所有这些方法都明确地鉴定出一个复杂程度约为1500个核苷酸的基因，该基因位于病毒RNA的3'端附近（Martin 1970; Wang et al. 1975; St6helin et al. 1976）。病毒复制不需要src，它的缺失会导致转化缺陷（td）突变体（Vogt 1971; Martin and Duesberg 1972）。在遗传杂交中，src分离具有转化功能（Wang et al. 1976b）。src-基因产物分子量（mw）为60,000，被认为具有磷酸激酶的功能（Brugge和Erikson 1977； Erikson等人；Bishop等人；均为本卷）。由于禽急性白血病病毒，包括禽红母细胞病病毒（AEV），禽髓细胞瘤病病毒MC29和CMII，米尔希尔病毒no。2 （MH2）和禽成髓细胞病病毒（AMV）通常在几天或几周内迅速引起特征性疾病，因此有理由认为它们与肉瘤病毒一样，含有负责转化的特定遗传信息，即onc基因，并且这些特定序列编码转化特异性蛋白质。由于急性白血病病毒在RNA肿瘤病毒（gag、/9ol和env）复制所必需的所有三个基因（Ishizaki和Shimizu 1970； Ishizaki等人1971；Bister等人1977；Bister和Vogt 1978）中存在广泛的缺陷，使用删除和重组分析来定义一个基因的遗传和生化方法尚不能应用（Duesberg，本卷）。然而，对几种急性白血病病毒株的rna的生化分析揭示了一种特殊的遗传结构。典型的急性白血病病毒的RNA约为6千碱基（kb），包含两组核苷酸序列：一组代表约40-60%的RNA，这是缺陷病毒所特有的；另一个代表RNA的剩余部分，这是群体特异性的，与禽肿瘤病毒组的非缺陷成员有关（Duesberg et al. 1977a; Mellon et al. 1978）。特异性序列和群特异性序列主要通过两种方法来区分。第一种方法利用缺陷病毒RNA与非缺陷病毒cDNA杂交来测量群特异性序列，并与缺陷病毒特异性cDNA杂交来测量特异性序列；第二种方法比较缺陷病毒的rnase - tl抗性寡核苷酸。
Based on their oncogenic properties, avian RNA tumor viruses have been divided into several classes:(1) sarcoma viruses, which cause solid tumors of the connective tissue in the animal;(2) acute leukemia viruses, which cause rapid hematopoietic disorders and malignancies, as well as renal and hepatic tumors, including carcinomas; and (3) lymphatic leukemia viruses, which cause lymphatic leukemias usually only after long latent periods (Purchase and Burmester 1972; Hanafusa 1977; Duesberg, this volume). There are, however, broad overlaps among the oncogenic spectra of these classes of viruses, in vivo and in vitro. Both sarcoma and acute leukemia viruses can transform fibroblasts in tissue culture, some of the acute leukemia viruses cause sarcomas in the animal, and sarcoma viruses occasionally induce erythroblastic leukemia (Purchase and Burmester 1972). Transformation by RNA tumor viruses is thought to be the consequence of a unique class of genes, termed onc genes (Baltimore 1975). The onc gene of Rous sarcoma virus (RSV) has been termed src (Wang et al. 1976a) to account for the predominant form of tumors induced by RSV. The definitiori and characterization of the src gene have been achieved using genetic as well as biochemical procedures. All of these approaches led to the unequivocal identification of a gene with a complexity of about 1500 nucleotides, which is located near the 3'end of viral RNA (Martin 1970; Wang et al. 1975; St6helin et al. 1976). src is not needed for viral replication and its deletion gives rise to transformation-defective (td) mutants (Vogt 1971; Martin and Duesberg 1972). In genetic crosses, src segregates with transforming function (Wang et al. 1976b). The src-gene product has a molecular weight (mw) of 60,000 and is thought to function as a phosphokinase (Brugge and Erikson 1977; Erikson et al.; Bishop et al.; both this volume). Since the avian acute leukemia viruses, including avian erythroblastosis virus (AEV), avian myelocytomatosis viruses MC29 and CMII, Mill Hill virus no. 2 (MH2), and avian myeloblastosis virus (AMV), cause characteristic diseases very rapidly usually within days or weeks, it is reasonable to assume that they, like the sarcoma viruses, contain specific genetic information responsible for transformation, ie, onc genes, and that these specific sequences code for transformationspecific proteins. Because of the extensive defectiveness of the acute leukemia viruses in all three genes essential for replication of RNA tumor viruses, gag,/9ol, and env (Ishizaki and Shimizu 1970; Ishizaki et al. 1971; Bister et al. 1977; Bister and Vogt 1978), genetic and biochemical approaches using deletion and recombination analyses for the definition of onc genes cannot as yet be applied (Duesberg, this volume). However, biochemical analyses of the RNAs of several strains of aviafi acute leukemia viruses reveal a characteristic genetic structure. The RNA of a typical acute leukemia virus measures about 6 kilobases (kb) and contains two sets of nucleotide sequences: one represents about 40-60% of the RNA, which is specific for the defective virus; the other represents the remainder of the RNA, which is group-specific and related to nondefective members of the avian tumor virus group (Duesberg et al. 1977a; Mellon et al. 1978).Specific and group-specific sequences are distinguished basically by two methods. The first method utilizes hybridization of defective viral RNA with cDNA of nondefective viruses to measure groupspecific sequences, and with defective virus-specific cDNA to measure specific sequences; the second method compares RNase-Tl-resistant oligonucleotides of defective viral …