Analysis of mutations in the envelope gene of Moloney murine leukemia virus: separation of infectivity from superinfection resistance.
Analysis of mutations in the envelope gene of Moloney murine leukemia virus: separation of infectivity from superinfection resistance.
复制标题
莫洛尼鼠白血病病毒包膜基因突变分析：感染性与重复感染抗性的分离。
DOI：
10.1016/0042-6822(91)90983-i
复制
发表时间：
1991
期刊：
影响因子：
3.7
通讯作者：
Goff,SP
中科院分区：
文献类型：
--
作者：
Granowitz,C;Colicelli,J;Goff,SP
在克隆的Moloney小鼠白血病病毒DNA拷贝的engene中产生了6个缺失突变和1个插入。通过NIH/3T3细胞转化检测，7个突变体均存在复制缺陷。将突变体dna导入NIH/3T3细胞，产生稳定的细胞系；所有的病毒粒子都释放到培养基中，这表明所有的突变都没有影响病毒基因的整体表达、基因和多基因的功能或病毒粒子的出芽。一些突变减少了env蛋白的寿命或阻止其向细胞表面输出。一个突变改变了TM蛋白的跨膜区和细胞质尾部，对蛋白质的输出、蛋白水解加工或与病毒粒子的结合没有影响，但仍然阻断了所产生的病毒的传染性。结果表明，跨膜区域的改变可以影响感染的早期步骤，如病毒粒子和宿主膜的融合。表达该突变蛋白的细胞对野生型病毒的重复感染具有完全的抗性。因此，病毒抗性的诱导（可能反映了病毒受体的阻断）可以与病毒感染性分离。
Six deletion mutations and an insertion were generated in theenvgene of cloned copies of Moloney murine leukemia virus DNA. All seven mutants were replication-defective as tested by transformation of NIH/3T3 cells. The mutant DNAs were introduced into NIH/3T3 cells to generate stable producer lines; all released virion particles into the medium, suggesting that none of the mutations affected overall viral gene expression,gagandpolgene functions, or virion budding. Several of the mutations reduced the lifetime of theenvprotein or blocked its export to the cell surface. One mutation altering the membrane-spanning region and the cytoplasmic tail of the TM protein had no effect on export of the protein, proteolytic processing, or incorporation into virion particles, but still blocked the infectivity of the resulting virus. The results suggest that alterations in the transmembrane region can affect early steps of infection, such as the fusion of virion and host membranes. Cells expressing this mutantenvprotein were fully resistant to superinfection by wild-type virus. Thus, induction of virus resistance, presumably reflecting blocking the virus receptor, can be separated from virus infectivity.