COMPLEMENTATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 VIF MUTANTS IN SOME CD4+ T-CELL LINES

被引:9
|
作者
HEVEY, M [1 ]
DONEHOWER, LA [1 ]
机构
[1] BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030
关键词
HUMAN IMMUNODEFICIENCY VIRUS; VIF; COMPLEMENTATION;
D O I
10.1016/0168-1702(94)90108-2
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The viral infectivity factor gene, vif of human immunodeficiency virus type 1 (HIV-1), is required for full infectivity in most T-cell lines. The replication kinetics exhibited by these mutants has been shown to be cell type-dependent. In H9 cells as well as primary lymphocytes, vif mutants are incapable of establishing infection. This has led to classification of these cell types as non-permissive for vif mutant replication. The T-cell lines Sup T1 and C8166 are able to replicate the vif mutant virus, leading to their classification as permissive for vif mutant replication. In this study, four cell lines (Sup T1, C8166, Molt 4 Clone 8, and A3.01) were tested for their ability to replicate vif mutant virus derived from two different strains of HIV-1 (HXB2 and NL4-3) that had been passaged on various cell lines. Although the kinetics of initial infection was delayed in all cells, by the second passage of vif mutant virus on Sup T1 or Molt 4 cells the kinetics of replication were identical to wild type virus. In contrast, mutant virus displayed delayed replication kinetics in C8166 and A3.01 cells in both initial and subsequent passages. In addition, the levels of viral DNA in infected Sup T1 cells were similar for Delta vif and wild type virus, but in C8166 cells Delta vif virus DNA levels were reduced compared to wild type virus. These results argue that in Sup T1 and Molt 4 cells there is a factor present that is able to complement the defect in vif mutant viruses which is absent or inefficient in its activity in C8166 and A3.01 cells.
引用
收藏
页码:269 / 280
页数:12
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