Li X, Mak J, Arts E J, Gu Z, Kleiman L, Wainberg M A, Parniak M A
Department of Medicine, Lady Davis Institute-Jewish General Hospital, Montreal, Quebec, Canada.
J Virol. 1994 Oct;68(10):6198-206. doi: 10.1128/JVI.68.10.6198-6206.1994.
The human immunodeficiency virus type 1 genomic RNA primer-binding site (PBS) sequence comprises 18 nucleotides which are complementary to those at the 3' end of the replication initiation primer tRNA(3Lys). To investigate the role of the PBS in viral replication, we either deleted the original wild-type PBS (complementary to tRNA(3Lys) or replaced it with DNA sequences complementary to either tRNA(1,2Lys) or tRNA(Phe). Transfection of COS cells with such molecular constructs yielded similar levels of viral progeny that were indistinguishable with regard to viral proteins and tRNA content. Virus particles derived from PBS-deleted molecular clones were noninfectious for MT-4, Jurkat, and CEM-T4 cells. However, infectious viruses were derived from constructs in which the PBS had been altered to sequences complementary to either tRNA(1,2Lys) or tRNA(Phe), although mutated forms showed significant lags in replication efficiency in comparison with wild types. Molecular analysis of reverse-transcribed DNA in cells infected by the mutated viruses indicated that both tRNA(1,2Lys) and tRNA(Phe) could function as primers for reverse transcription during the early stages of infection. Sequencing of full-length proviral DNA, obtained 6 days after infection, revealed the mutated PBS, indicating that a complete cycle of reverse transcription had occurred. During subsequent rounds of infection, reversion of the mutated PBS to wild-type sequences was observed, accompanied by increased production of viral gene products. Reversion to wild-type PBS sequences was confirmed both by specific PCR analysis, using distinct primer pairs, and by direct sequencing of amplified segments. We also performed endogenous in vitro reverse transcription experiments in which synthesis of minus-strand strong-stop viral DNA was primed from a synthetic RNA template containing a PBS complementary to various tRNA isoacceptors. These results showed that tRNA(3Lys) was a much more efficient primer of such reactions than either tRNA(1,2Lys) or tRNA(Phe).
1型人类免疫缺陷病毒基因组RNA引物结合位点(PBS)序列由18个核苷酸组成,与复制起始引物tRNA(3Lys) 3'端的核苷酸互补。为了研究PBS在病毒复制中的作用,我们要么删除了原始的野生型PBS(与tRNA(3Lys)互补),要么用与tRNA(1,2Lys)或tRNA(Phe)互补的DNA序列取代它。用这些分子构建体转染COS细胞产生了相似水平的病毒后代,在病毒蛋白和tRNA含量方面没有区别。来自PBS缺失分子克隆的病毒颗粒对MT-4、Jurkat和CEM-T4细胞无感染性。然而,感染性病毒来自PBS已被改变为与tRNA(1,2Lys)或tRNA(Phe)互补序列的构建体,尽管与野生型相比,突变形式在复制效率上有明显滞后。对被突变病毒感染的细胞中逆转录DNA的分子分析表明,tRNA(1,2Lys)和tRNA(Phe)在感染早期都可以作为逆转录的引物。感染6天后获得的全长前病毒DNA测序显示了突变的PBS,表明发生了完整的逆转录循环。在随后的感染轮次中,观察到突变的PBS恢复为野生型序列,同时病毒基因产物的产量增加。通过使用不同引物对的特异性PCR分析以及对扩增片段的直接测序,证实了恢复为野生型PBS序列。我们还进行了内源性体外逆转录实验,其中负链强终止病毒DNA的合成是从含有与各种tRNA同工受体互补的PBS的合成RNA模板引发的。这些结果表明,tRNA(3Lys)比tRNA(1,2Lys)或tRNA(Phe)更有效地引发此类反应。