ID SEQUENCE ELEMENT ABOVE POLYPURINE TRACT ESSENTIAL FOR SIV REPLICATION
ID SEQUENCE ELEMENT ABOVE POLYPURINE TRACT ESSENTIAL FOR SIV REPLICATION
批准号:
6453746
负责人:
PETR O ILYINSKII
金额:
$11.11万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-05-01 至 2002-04-30
中文摘要
紧靠其上游的一小段富T序列
多聚尿路(PPT)在猪瘟病毒前病毒基因组中高度保守
人类和猿类免疫缺陷病毒(HIV和SIV)调查
这个“U盒”是否会影响SIVmac239复制,我们分析了
病毒基因组这个区域发生变化的突变体的特性
所有突变体要么生长迟缓(长达一个月)
延迟)或未在CEMx174细胞中检测到复制
突变体确实可以检测到复制,补偿性变化
在病毒基因组中一直观察到最常见的代偿性
变化是胸腺嘧啶的获得立即上游
Ppt,但也观察到PPT长度的显著扩张
通过转染法瞬时产生的U-box突变体严重
他们产生逆转录本的能力受损
瞬时产生的突变病毒的感染性分析
这些结果显示在RNA包装或病毒组装方面没有缺陷
确定新的结构元素,这对早期的
包括逆转录出版物在内的病毒生命周期
Ilyinskii,PO和Desrosiers,一个序列元件的RC鉴定
就在多聚尿路的上游,这对
猴免疫缺陷病毒的复制EMBO J 1998;17:3766-3774
英文摘要
A short stretch of T-rich sequences immediately upstream of the
polypurine tract (PPT) is highly conserved in the proviral genomes of
human and simian immunodeficiency viruses (HIV and SIV) To investigate
whether this "U-box" influences SIVmac239 replication, we analyzed the
properties of mutants with changes in this region of the viral genome
All mutants were either retarded in their growth (up to one month
delay) or did not replicate detectably in CEMx174 cells When U-box
mutants did replicate detectably, compensatory changes were
consistently observed in the viral genome The most common compensatory
change was the acquisition of thymidines immediately upstream of the
PPT, but marked expansion in the length of the PPT was also observed
U-box mutants produced transiently by transfection were severely
impaired in their ability to produce reverse transcripts in
infectivity assays Analysis of transiently produced mutant virus
revealed no defect in RNA pack agin g or virus assembly These results
identify a new structural element important for an early step in the
viral life cycle that includes reverse transcription PUBLICATIONS
Ilyinskii, PO and Desrosiers, RC Identification of a sequence element
immediately upstream of the polypurine tract that is essential for
replication of simian immunodeficiency virus EMBO J 1998; 17:3766-3774
期刊论文(0)
专著(0)
科研奖励(0)
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海外基金