Hevey M, Donehower L A
Division of Molecular Virology, Baylor College of Medicine, Houston, TX 77030.
Virus Res. 1994 Sep;33(3):269-80. doi: 10.1016/0168-1702(94)90108-2.
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.
人类免疫缺陷病毒1型(HIV-1)的病毒感染性因子基因vif,是大多数T细胞系实现完全感染性所必需的。已证明这些突变体表现出的复制动力学是细胞类型依赖性的。在H9细胞以及原代淋巴细胞中,vif突变体无法建立感染。这导致这些细胞类型被归类为对vif突变体复制不许可。T细胞系Sup T1和C8166能够复制vif突变病毒,因此被归类为对vif突变体复制许可。在本研究中,测试了四种细胞系(Sup T1、C8166、Molt 4克隆8和A3.01)复制源自两种不同HIV-1毒株(HXB2和NL4-3)且已在各种细胞系上传代的vif突变病毒的能力。尽管在所有细胞中初始感染的动力学都有所延迟,但vif突变病毒在Sup T1或Molt 4细胞上第二代传代时,其复制动力学与野生型病毒相同。相比之下,突变病毒在C8166和A3.01细胞的初始和后续传代中均表现出延迟的复制动力学。此外,感染的Sup T1细胞中δvif病毒和野生型病毒的病毒DNA水平相似,但在C8166细胞中,δvif病毒DNA水平与野生型病毒相比有所降低。这些结果表明,在Sup T1和Molt 4细胞中存在一种因子,能够弥补vif突变病毒的缺陷,而这种因子在C8166和A3.01细胞中不存在或活性不足。