Nagy P D, Carpenter C D, Simon A E
Department of Biochemistry and Molecular Biology, University of Massachusetts, Amherst 01003, USA.
Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1113-8. doi: 10.1073/pnas.94.4.1113.
Many positive-stranded RNA viruses contain short, single-stranded 3' ends that are vulnerable to degradation by host cellular RNases. Therefore, the existence of a 3'-end repair mechanism (analogous to cellular telomerases) must be required and/or advantageous for RNA viruses. Accordingly, we provide evidence suggesting that deletions of up to 6 nt from the 3' end of satellite (sat-) RNA C (a small parasitic RNA associated with turnip crinkle carmovirus) are repaired to the wild-type sequence in vivo and in vitro. The novel 3'-end repair mechanism involves the production of 4-8 nt oligoribonucleotides by abortive synthesis by the viral replicase using the 3' end of the viral genomic RNA as template. Based on our in vitro results, we postulate that the oligoribonucleotides are able to prime synthesis of wild-type negative-strand sat-RNA C in a reaction that does not require base pairing of the oligoribonucleotides to the mutant, positive-strand RNA template. The discovery of a 3'-end repair mechanism opens up new strategies for interfering with viral infections.
许多正链RNA病毒含有短的单链3'末端，这些末端容易被宿主细胞核糖核酸酶降解。因此，对于RNA病毒来说，3'末端修复机制（类似于细胞端粒酶）的存在必定是必需的和/或有益的。相应地，我们提供的证据表明，卫星（sat-）RNA C（一种与芜菁皱缩病毒相关的小寄生RNA）3'末端多达6个核苷酸的缺失在体内和体外都能修复为野生型序列。这种新的3'末端修复机制涉及病毒复制酶以病毒基因组RNA的3'末端为模板通过流产合成产生4 - 8个核苷酸的寡核糖核苷酸。基于我们的体外实验结果，我们推测这些寡核糖核苷酸能够在一个不需要寡核糖核苷酸与突变的正链RNA模板进行碱基配对的反应中引发野生型负链sat-RNA C的合成。3'末端修复机制的发现为干扰病毒感染开辟了新的策略。
