Are spleen focus-forming virus sequences related to xenotropic viruses and expressed specifically in normal erythroid cells?
Are spleen focus-forming virus sequences related to xenotropic viruses and expressed specifically in normal erythroid cells?
复制标题
脾病灶形成病毒序列是否与异种病毒相关并在正常红细胞中特异性表达？
作者：
I. Pragnell;A. McNab;P. R. Harrison;W. Osterag
缺陷性C型RNA肿瘤病毒是亲嗜性和异嗜性病毒之间的基因重组体，已被描述并被认为是病毒诱导的淋巴性白血病过程中的真实的转化剂1，2。Friend病毒（FV）复合物的脾病灶形成病毒（SFFV-F）组分是一种缺陷病毒，是该复合物的红系特异性组分，可刺激小鼠红细胞生成，也参与相对罕见的红系转化事件3，4。为了检查SFFV组分在成红细胞增多症和随后的红系细胞转化过程中的作用，我们使用从F4 - 6（转化的红系细胞系）释放的FV合成了SFFV特异性探针5，6。我们在这里报告说，使用这种探针，没有异嗜性序列中存在的SFFV特异性的cDNA和有一个低水平的转录的SFFV序列的一部分，但不是特别是在正常的红细胞分化。因此，我们的研究结果表明，如果SFFV是一种重组病毒，异嗜性序列只存在于淋巴白血病病毒（LLV）相关的FV基因组的共同序列。此外，我们的实验不支持SFFV的特异性作用可以通过SFFV特异性基因组在正常红系分化过程中的转录来解释的假设。
DEFECTIVE type C RNA tumour viruses which are genetic recombinants between ecotropic and xenotropic viruses have been described and suggested to be the real transforming agents during the course of viral-induced lymphatic leukaemia1,2. The spleen focus-forming virus (SFFV-F) component of the Friend virus (FV) complex is a defective virus and is the erythroid-specific component of the complex which stimulates erythropoiesis in the mouse and is also involved in the relatively rare event of erythroid transformation3,4. In order to examine the role of the SFFV component during erythroblastosis and subsequent transformation of erythroid cells, we have synthesised a SFFV-specific probe using FV released from F4-6, a transformed erythroid cell line5,6. We report here that, using this probe, no xenotropic sequences are present in the SFFV-specific cDNA and that there is a low level of transcription of part of the SFFV sequences but not specifically during normal erythroid differentiation. Our results thus show that if SFFV is a recombinant virus, the xenotropic sequences are only present in the lymphatic leukaemia virus (LLV)-related common sequences of the FV genome. Furthermore, our experiments do not support a hypothesis whereby the specific action of SFFV can be explained by transcription of the SFFV-specific genome during normal erythroid differentiation.