Genetic structure of avian myeloblastosis virus, released from transformed myeloblasts as a defective virus particle.
Genetic structure of avian myeloblastosis virus, released from transformed myeloblasts as a defective virus particle.
复制标题
禽成髓细胞瘤病毒的遗传结构，从转化的成髓细胞中作为有缺陷的病毒颗粒释放。
DOI：
10.1073/pnas.77.9.5120
复制
发表时间：
1980
影响因子：
11.1
通讯作者：
Moscovici,C
中科院分区：
文献类型：
--
作者：
Duesberg,PH;Bister,K;Moscovici,C
在无缺陷辅助病毒的情况下，用禽成髓细胞瘤病毒（AMV）转化鸡成髓细胞（称为非生产细胞），发现其释放出含有禽肿瘤病毒囊蛋白但缺乏包膜糖蛋白和DNA聚合酶的缺陷病毒颗粒（DVP）。非生产细胞含有Pr 76 gag前体蛋白，也含有一种与非缺陷病毒的Pr 180 gag-polprotein无法区分的蛋白。DVP的RNA长7.5 kb，比辅助病毒AMV、MAV-1和MAV-2的8.2 kb RNA短0.7 kb。RNA·cDNA杂交和RNase T1抗性寡核苷酸图谱的比较表明，DVP RNA与MAV的5′-端有5.3kb的同源序列，而3′-端有0.7kb的C区，这与其它禽肿瘤病毒不同。DVP RNA与C区相邻，含有由14个特异性寡核苷酸限定的1.5 kb的连续特异性序列。除了其中两个寡核苷酸在其5′端作图外，该序列与4个不同包膜亚群的无缺陷禽肿瘤病毒的任何序列以及4个不同RNA亚群的成纤维细胞转化禽急性白血病和肉瘤病毒的特异性序列都不相关。DVP RNA的特异性序列存在于本实验室和其他实验室的AMV感染性原种中，存在于另一个实验室的AMV转化的成髓细胞系中，并且它与E26病毒（AMV样病毒的独立分离株）的核苷酸序列约70%相关。初步实验表明，如果在辅助病毒存在下融合到易感细胞中，DVP是致白血病的。我们的结论是，DVP RNA是白血病的传染性AMV的组成部分，其特定的序列，termedAMV，可能携带致癌性的遗传信息。因此，我们在这里发现了一个转化特异性RNA序列，与辅助病毒无关，在一个高度致癌的病毒，不转化成纤维细胞。
Chicken myeloblasts transformed by avian myeloblastosis virus (AMV) in the absence of nondefective helper virus (termed nonproducer cells) were found to release a defective virus particle (DVP) that contains avian tumor viralgagproteins but lacks envelope glycoprotein and a DNA polymerase. Nonproducer cells contain a Pr76gagprecursor protein and also a protein that is indistinguishable from the Pr180gag-polprotein of nondefective viruses. The RNA of the DVP is 7.5 kilobases (kb) long and is 0.7 kb shorter than the 8.2-kb RNAs of the helper viruses of AMV, MAV-1 and MAV-2. Comparisons based on RNA·cDNA hybridization and mapping of RNase T1-resistant oligonucleotides indicated that DVP RNA shares with MAV RNAs nearly isogenic 5′-terminalgagandpol-related sequences of 5.3 kb and a 3′-terminal c-region of 0.7 kb that is different from that found in other avian tumor viruses. Adjacent to the c-region, DVP RNA contains a contiguous specific sequence of 1.5 kb defined by 14 specific oligonucleotides. Except for two of these oligonucleotides that map at its 5′ end, this sequence is unrelated to any sequences of nondefective avian tumor viruses of four different envelope subgroups as well as to the specific sequences of fibroblast-transforming avian acute leukemia and sarcoma viruses of four different RNA subgroups. The specific sequence of the DVP RNA is present in infectious stocks of AMV from this and other laboratories in an AMV-transformed myeloblast line from another laboratory, and it is about 70% related to nucleotide sequences of E26 virus, an independent isolate of an AMV-like virus. Preliminary experiments show DVP to be leukemogenic if fused into susceptible cells in the presence of helper virus. We conclude that DVP RNA is the leukemogenic component of infectious AMV and that its specific sequence, termedAMV, may carry genetic information for oncogenicity. Thus we have found here a transformation-specific RNA sequence, unrelated to helper virus, in a highly oncogenic virus that does not transform fibroblasts.