Kim T, Mudry R A, Rexrode C A, Pathak V K
Department of Biochemistry and Mary Babb Randolph Cancer Center, West Virginia University, Morgantown 26506, USA.
J Virol. 1996 Nov;70(11):7594-602. doi: 10.1128/JVI.70.11.7594-7602.1996.
Retroviruses mutate at a high rate in vivo during viral replication. Mutations may occur during proviral transcription by RNA polymerase II, during minus-strand DNA synthesis (RNA template) by viral reverse transcriptase, or during plus-strand DNA synthesis (DNA template) by reverse transcriptase. To determine the contributions of different stages of replication to the retroviral mutation rates, we developed a spleen necrosis virus-based in vivo system to selectively identify mutations occurring during the early stage (RNA transcription plus minus-strand synthesis) and the late stage (plus-strand synthesis plus DNA repair). A lacZalpha reporter gene was inserted into the long terminal repeat (LTR) of a spleen necrosis virus shuttle vector, and proviruses were recovered from infected cells as plasmids containing either one or both LTRs. Plasmids containing both LTRs generated a mutant phenotype only if the lacZalpha genes in both LTRs were mutated, which is most likely to occur during the early stage. Mutant phenotypes were identified from plasmids containing one LTR regardless of the stage at which the mutations occurred. Thus, mutant frequencies obtained after recovery of plasmids containing both LTRs or one LTR provided early-stage and total mutation rates, respectively. Analysis of 56,409 proviruses suggested that the retroviral mutation rates during the early and late stages of replication were equal or within twofold of each other. In addition, two mutants with A-to-G hypermutations were discovered, suggesting a role for mammalian double-stranded RNA adenosine deaminase enzyme in retroviral mutations. These experiments provide a system to selectively identify mutations in the early stage of retroviral replication and to provide upper and lower limits to the in vivo mutation rates during minus-strand and plus-strand synthesis, respectively.
逆转录病毒在体内病毒复制过程中突变率很高。突变可能发生在原病毒转录过程中(由RNA聚合酶II进行)、负链DNA合成过程中(以RNA为模板,由病毒逆转录酶进行)或正链DNA合成过程中(以DNA为模板,由逆转录酶进行)。为了确定复制不同阶段对逆转录病毒突变率的贡献,我们开发了一种基于脾坏死病毒的体内系统,以选择性地鉴定早期阶段(RNA转录加负链合成)和晚期阶段(正链合成加DNA修复)发生的突变。将一个lacZα报告基因插入脾坏死病毒穿梭载体的长末端重复序列(LTR)中,从感染细胞中回收的原病毒作为含有一个或两个LTR的质粒。只有当两个LTR中的lacZα基因都发生突变时,含有两个LTR的质粒才会产生突变表型,这最有可能发生在早期阶段。无论突变发生在哪个阶段,都可以从含有一个LTR的质粒中鉴定出突变表型。因此,回收含有两个LTR或一个LTR的质粒后获得的突变频率分别提供了早期阶段和总突变率。对56409个原病毒的分析表明,逆转录病毒在复制早期和晚期的突变率相等或相差不超过两倍。此外,还发现了两个具有A到G超突变的突变体,这表明哺乳动物双链RNA腺苷脱氨酶在逆转录病毒突变中发挥了作用。这些实验提供了一个系统,用于选择性地鉴定逆转录病毒复制早期的突变,并分别为负链和正链合成过程中的体内突变率提供上限和下限。