An intact U5-leader stem is important for efficient replication of simian immunodeficiency virus.
An intact U5-leader stem is important for efficient replication of simian immunodeficiency virus.
复制标题
完整的 U5 前导茎对于猿猴免疫缺陷病毒的有效复制非常重要。
DOI：
10.1128/jvi.75.23.11924-11929.2001
复制
发表时间：
2001
影响因子：
5.4
通讯作者：
Wainberg,MA
中科院分区：
文献类型：
--
作者：
Guan,Y;Diallo,K;Whitney,JB;Liang,C;Wainberg,MA
先前的研究表明，猴免疫缺陷病毒（SIV）中的四种缺失，称为SD 1a，SD 1b，SD 1c和SD 6，分别消除了位于引物结合位点下游的核苷酸位置322至362，322至370，322至379和371至379处的序列，不同程度地损害了病毒的复制能力。含有SD 1a、SD 1b和SD 6缺失的病毒的长期培养导致具有野生型复制动力学的回复突变体。我们现在表明，这些回复突变体在每种情况下都保留了原始的缺失，但也存在新的额外突变。这些包括U 5区域内称为D1（nt +216至+237）的大缺失，其显示与SD 1a和SD 1b构建体的回复具有生物学相关性。在SD 6的情况下，两个补偿性点突变，即，A+369 G（称为M1）位于SD 6缺失的上游，C+201 T（称为M2）位于U 5内，可以单独或联合作用以恢复病毒复制。二级结构表明，一个完整的U 5-前导茎是重要的SIV的感染性和描述的其他突变体在恢复这一主题发挥了重要作用。
Previous work has shown that four deletions in simian immunodeficiency virus (SIV), termed SD1a, SD1b, SD1c, and SD6, which eliminated sequences at nucleotide positions 322 to 362, 322 to 370, 322 to 379, and 371 to 379, respectively, located downstream of the primer binding site, impaired viral replication capacity to different extents. Long-term culturing of viruses containing the SD1a, SD1b, and SD6 deletions led to revertants that possessed wild-type replication kinetics. We now show that these revertants retained the original deletions in each case but that novel additional mutations were also present. These included a large deletion termed D1 (nt +216 to +237) within the U5 region that was shown to be biologically relevant to reversion of both the SD1a and SD1b constructs. In the case of SD6, two compensatory point mutations, i.e., A+369G, termed M1, located immediately upstream of the SD6 deletion, and C+201T, termed M2, within U5, were identified and could act either singly or in combination to restore viral replication. Secondary structure suggests that an intact U5-leader stem is important in SIV for infectiousness and that the additional mutants described played important roles in restoration of this motif.