Yao W, Bruenn J A
Department of Biological Sciences, SUNY/Buffalo 14260, USA.
Virology. 1995 Dec 1;214(1):215-21. doi: 10.1006/viro.1995.9938.
It is possible to interfere with the replication of a number of plant RNA viruses by systemic production of viral capsid polypeptides or RNA-dependent RNA polymerases, or by production of untranslatable portions of viral plus strands or minus strands. Interference can occur by a number of mechanisms. We have discovered that the Saccharomyces cerevisiae double-stranded RNA viruses ScVL1 and ScVLa, which exist as permanent persistent infections of their host cells, can be cured very efficiently by production of N-terminal fragments of their capsid polypeptides. These totiviruses produce only two polypeptides: a capsid polypeptide (Cap) and a Cap-Pol fusion polypeptide with RNA-dependent RNA polymerase activity. Three types of interference can be detected: interference due to overproduction of both Cap and Cap-Pol, interference due to overproduction of Cap (and consequent distortion of the Cap to Cap-Pol ratio), and interference due to negative complementation by N-terminal fragments of Cap. Some N-terminal fragments of Cap appear to be incorporated into viral particles, but only in the presence of a complete Cap protein. We postulate that incorporation of N-terminal fragments of Cap results in the formation of defective particles.
通过系统性产生病毒衣壳多肽或RNA依赖性RNA聚合酶，或通过产生病毒正链或负链的不可翻译部分，有可能干扰多种植物RNA病毒的复制。干扰可通过多种机制发生。我们发现，酿酒酵母双链RNA病毒ScVL1和ScVLa作为其宿主细胞的永久性持续感染存在，通过产生其衣壳多肽的N端片段可以非常有效地治愈。这些全病毒仅产生两种多肽：一种衣壳多肽（Cap）和一种具有RNA依赖性RNA聚合酶活性的Cap-Pol融合多肽。可以检测到三种类型的干扰：由于Cap和Cap-Pol的过量产生导致的干扰、由于Cap的过量产生（以及随之而来的Cap与Cap-Pol比例的扭曲）导致的干扰，以及由于Cap的N端片段的负互补导致的干扰。Cap的一些N端片段似乎被整合到病毒颗粒中，但仅在存在完整Cap蛋白的情况下。我们推测Cap的N端片段的整合导致缺陷颗粒的形成。
