中文摘要：

基于全身的传染 cDNA 克隆，中国人孤立的烟草坏死病毒的基因修正(TNV -- ^C ) 被指导地点的傻瓜发育不全或核苷酸删除做为在变异的病毒的 RNA 的 vitro 抄写。Chenopodium amaranticolor 与的机械接种在 vitro 抄本，为二 subgenomic (sg ) 在假定 transcriptional 开始地点包含单个 nucleic 替换 RNA，证明 TNV 的 sgRNA1 和 sgRNA2 -- ^C 分别地在 G ²¹⁸⁴ 或 G ²⁴⁶⁰, 被开始。为 P8 或 P6 由 sgRNA1 编码了的开读物的框架(ORF ) 的翻译 initiation-codons 的 Mutagenesis 显示每二基因为 C 上的本地损害的形成是必要的。amaranticolor 叶子，也许由堵住病毒 cell-to-cell 运动，但是不为在烟草房间 BY-2 的原物的病毒的 RNA 是必要的。原核生物的表示的结果证明在 TNV 上为上衣蛋白质编码的 ORF -- ^C sgRNA2 被第一条 8 月鳕鱼创始地翻译在上在核苷酸 2612 2614。翻译开始鳕鱼 ons 的指导地点的变化，和全部编码区域的删除，证明未经触动的 TNV -- ^C 上衣蛋白质为 TNV 的建立是非必需的 -- ^{在 C 的 C} 感染。amaranticolor 否则本地损害和病毒的 RNA 累积水平的数字被减少，或症状外观的时间显著地推迟了。这些结果建议核苷酸在为 TNV 编码上在翻译开始鳕鱼附近定序 -- ^C 上衣蛋白质基因可以在本地症状起一个重要作用。在 TNV 的上衣蛋白质的参与的方面 -- ^C 生命周期被讨论。

英文摘要：

Based on a full-length infectious cDNA clone, gene modifications of Tobacco necrosis virus A Chinese isolate （TNV-Ac） were made by site-directed mutagenesis or nucleotide deletions for in vitro transcription of mutant viral RNAs. Mechanical inoculations of Chenopodium amaranticolor with in vitro transcripts, containing a single nucleic acid substitution at the presumed transcriptional start sites for the two subgenomic （sg） RNAs, showed that the sgRNA1 and sgRNA2 of TNV-A^c were initiated at G^2184 or G^2460, respectively. Mutagenesis of the translational initiation-codons for the open-reading frame （ORF） P8 or P6 encoded by sgRNA1 indicated that each of the two genes was essential for formation of local lesions on C. amaranticolor leaves, perhaps by blocking virus cell-to-cell movement, but were not necessary for viral RNA replication in the protoplast of tobacco cell BY-2. Results of prokaryotic expression showed that the ORF coding for coat protein on TNV-Ac sgRNA2 was initiatively translated by the first AUG codon at nucleotides 2612--2614. Site-directed mutation of translational start codons, and deletion of the entire coding region, showed that the intact TNV-Ac coat protein was dispensable for establishment of TNV-A^c infection in C. amaranticolor, otherwise the numbers of local lesions and the viral RNA accumulation level were reduced, or the time to symptom appearance significantly delayed. These results suggested that the nucleotide sequence around the translational start codon coding for TNV-A^c coat protein gene may play an important role in the local symptoms. Aspects of the involvement of the coat protein in the TNV-A^c life cycle were discussed.