Krohn K J, Hakkarainen K, Aavik E, Dewhurst S, Sadaie R, Mullins J I
Institute of Biomedical Sciences, University of Tampere, Finland.
J Virol. 1993 Sep;67(9):5681-4. doi: 10.1128/JVI.67.9.5681-5684.1993.
A molecular clone of the simian immunodeficiency virus SIVSMM isolate PBj14, lacking the ATG initiation codon for Rev protein (PBj-1.5), did not produce virus or large unspliced or singly spliced viral RNA upon transfection of HeLa cells. Low but significant levels of virus and large viral RNA production were observed upon transfection of PBj-1.5 into HeLa Rev cells expressing the rev gene of human immunodeficiency virus type 1. Furthermore, abundant virus and large viral RNA production occurred upon transfection of PBj-1.5 into HeLa Rex cells expressing the rex gene of human T-cell leukemia virus type I. Virus produced from HeLa Rex and HeLa Rev transfections was infectious, produced large amounts of virus, and was cytopathic for Rex-producing MT-4 cells. In contrast, no or only low levels of virus production were observed upon infection of H9 cells. These studies show that a defective SIV rev gene can be transcomplemented with human immunodeficiency virus type 1 Rev and with high efficiency by human T-cell leukemia virus type I Rex, and they suggest that rev-defective viruses could serve as a source for production of a live attenuated SIV vaccine.
猿猴免疫缺陷病毒SIVSMM分离株PBj14的分子克隆体（PBj-1.5）缺少Rev蛋白的ATG起始密码子，在转染HeLa细胞后不产生病毒，也不产生大量未剪接或单剪接的病毒RNA。将PBj-1.5转染到表达人免疫缺陷病毒1型rev基因的HeLa Rev细胞中时，观察到低水平但显著的病毒和大量病毒RNA产生。此外，将PBj-1.5转染到表达人T细胞白血病病毒I型rex基因的HeLa Rex细胞中时，会产生大量病毒和大量病毒RNA。从HeLa Rex和HeLa Rev转染产生的病毒具有传染性，能产生大量病毒，并且对产生Rex的MT-4细胞具有细胞病变作用。相比之下，感染H9细胞后未观察到病毒产生或仅观察到低水平的病毒产生。这些研究表明，有缺陷的SIV rev基因可以被人免疫缺陷病毒1型Rev反式互补，并且能被人T细胞白血病病毒I型Rex高效反式互补，这表明rev缺陷病毒可作为生产减毒活SIV疫苗的来源。
