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首页> 外文期刊>Journal of Virology >Reduced leukemogenicity caused by mutations in the membrane glycoprotein gene of Rauscher spleen focus-forming virus.
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Reduced leukemogenicity caused by mutations in the membrane glycoprotein gene of Rauscher spleen focus-forming virus.

机译：通过Rauscher脾脏聚焦成对病毒的膜糖蛋白基因突变引起的白血病性降低。

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摘要

We isolated and characterized two spontaneous, weakly leukemogenic mutants of Rauscher spleen focus-forming virus (R-SFFV) that contain mutations in nonoverlapping regions of the membrane envelope (env) glycoprotein gene. As reported previously (M. Ruta and D. Kabat, J. Virol. 35:844-853, 1980), the replication-defective R-SFFV encodes a membrane glycoprotein with an apparent Mr of 54,000 (gp54) which is structurally and immunologically related to the membrane envelope glycoproteins of dual-tropic murine leukemia viruses. Mutant R-SFFV clones 3-25 and 4-3 encode abnormally sized gp54-related glycoproteins with apparent Mrs of 52,000 (gp52) and 45,000 (gp45), respectively. Northern and Southern blot analyses of the mutant R-SFFV nucleic acids indicated that an insertion has occurred in the 3-25 env gene and that a deletion has occurred in the 4-3 env gene. Furthermore, restriction endonuclease analyses and comparisons of the fragmentation patterns of the wild-type and mutant glycoproteins generated by partial proteolysis with Staphylococcus aureus V8 protease indicated that the mutations affect nonoverlapping domains of the envelope glycoprotein (amino-terminal fragment affected in 3-25 glycoprotein and carboxyl-terminal fragment affected in 4-3 glycoprotein). Glycosylation inhibition studies indicated that the reduced size of gp52 is caused at least partly by loss of an asparagine-linked oligosaccharide. In addition, these mutant viruses have dramatically reduced leukemogenicities compared with wild-type R-SFFV. We conclude that the gp54 structural gene is required for initiation or amplification of the splenic erythroblast hyperplasia which characterizes the preleukemic phase of Rauscher disease.
机译：我们被隔离并表征了葡萄糖脾脏聚焦形成病毒（R-SFFV）的两种自发性弱白血动突变体，其含有膜封套（ENV）糖蛋白基因的非突出区域中的突变。如前所述（M. Ruta和D.Kabat，J.Virol。35：844-853,980），复制缺陷的R-SFFV在结构上和免疫的表观MR为54,000（GP54）的表观MR中编码膜糖蛋白与双热带鼠白血病病毒的膜包膜糖蛋白有关。突变体R-SFFV克隆3-25和4-3分别用明显的MR为52,000（GP52）和45,000（GP45）对异常大小的GP54相关糖蛋白编码。突变体R-SFFV核酸的北部和Southern印迹分析表明，在3-25 env基因中发生插入，并且在4-3个Env基因中发生缺失。此外，限制性内切核酸酶分析和通过部分蛋白溶血气体V8蛋白酶产生的野生型和突变糖蛋白的碎片模式的分析和比较表明，突变影响包膜糖蛋白的非粘接结构域（在3-25糖蛋白中受影响的氨基 - 末端片段在4-3糖蛋白中影响羧基末端片段）。糖基化抑制研究表明，GP52的减小尺寸至少部分地引起了天冬酰胺连接的寡糖。此外，与野生型R-SFFV相比，这些突变病毒显着降低了白血病。我们得出结论，GP54结构基因是开始或扩增脾肠细胞增生，其表征Rauscher病的前期血症阶段。

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