THE RRE OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 CONTRIBUTES TO CELL-TYPE-SPECIFIC VIRAL TROPISM

被引:10
作者
DAYTON, ET
KONINGS, DAM
LIM, SY
HSU, RKS
BUTINI, L
PANTALEO, G
DAYTON, AI
机构
[1] NIAID,BETHESDA,MD 20892
[2] HARVARD UNIV,SCH MED,BOSTON,MA 02115
[3] UNIV COLORADO,DEPT MOLEC CELLULAR & DEV BIOL,BOULDER,CO 80309
[4] UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48109
[5] IST CLIN MED,ANCONA,ITALY
关键词
D O I
10.1128/JVI.67.5.2871-2878.1993
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
As part of a general program investigating the mechanism of the Rev axis of human immunodeficiency virus type 1 (HIV-1) autoregulation, a series of proviral HIV-1 mutants which differ from the parental HXB2 strain at selected positions within the RRE were constructed. All of the mutations were designed to perturb the RRE by introducing local helix disruptions without altering the coding potential of the overlapping envelope open reading frame. Viral replication in various cell types was monitored by a cell supernatant reverse transcriptase assay and Northern (RNA blot) analysis. All proviral RRE mutants displayed at least some impairment in replication. However, the relative impairment varied drastically among the various cell types tested. This suggests that the RRE may contribute to cell-type-specific viral tropism.
引用
收藏
页码:2871 / 2878
页数:8
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