The Role of 5' ICR Sequences in Viral (+) RNA Replication

大多数病毒性疾病，人，他的牲畜，和作物， 是由RNA病毒引起的 尽管有明显的 重要的是，对分子的了解非常少。 RNA病毒复制的过程。 重组DNA 技术已经提供了用于解决 问题之一是基因工程的能力 病毒RNA的拷贝。 RNA在体外的转录 野生型病毒序列的cDNA，在一些情况下， 产生感染性RNA。 在cDNA水平上的突变是 相对容易，和RNA转录的这种改变克隆 可以作为RNA水平上的特异性突变体。 序列 与tRNA的内部启动子惊人相似 基因，内部控制区（ICR），也称为A和B 盒，最近被观察到在5'末端的 雀麦花叶病毒（BMV）和其它病毒的基因组RNA。 5'末端位置，它们与 最近表征的亚基因组核心序列 启动子，并进行了BMV基因组RNA 3的缺失分析 提供了强有力的间接证据证明 作为（+）链复制的启动子起作用。 主要研究者有 使用野生型和突变体转录物与 独特的体外复制程序来定义 基因组（-）链合成和亚基因组（+） 链合成 然而，（+）链的启动子 基因组RNA合成尚未确定。 体内病毒 RNA合成通常是高度不对称的， 合成的（+）链RNA多于（-）链。n tRNA 真核生物中依赖于聚合酶III的基因转录 和相关的转录因子，是一个核过程。 与tRNA启动子的表观同源性表明 宿主因子参与病毒（+）链合成， 提出了可能的pol III转录因子。 实验是为了确定哪些元素， 在BMV的ICR周围， 复制的 此外，国际民事代表在 复制的不对称性，并在确定具体的 合成的基因组RNA的摩尔比。 识别复制中涉及的宿主因子 因为它们是宿主病原体的核心 关系

Most viral diseases, of man, his livestock, and crops are caused by viruses having RNA genomes. Despite the obvious importance, remarkably little is known about the molecular processes of RNA viral replication. Recombinant DNA techniques have provided procedures for addressing the problem, one of these being the ability to engineer cDNA copies of viral RNAs. Transcription of RNA in vitro from cDNAs of wild-type viral sequences has, in several cases, yielded infectious RNA. Mutagenesis at the cDNA level is relatively facile, and RNA transcripts of such altered clones can serve as specific mutants at the RNA level. Sequences with striking resemblance to the internal promoters of tRNA genes, internal control regions (ICRs), also termed A and B boxes, have recently been observed at the 5' termini of the genomic RNAs of brome mosaic virus (BMV)and other viruses. The 5' terminal location, their partial homology to the recently characterized core sequence f the subgenomic promoter, and the deletion analysis of BMV genomic RNA3 provide strong circumstantial evidence that these sequenced function as promoters of (+) strand replication. The Pi has used wild type and mutant transcripts in combination with unique in vitro replication procedures to define the promoters of genomic (-) strand synthesis and subgenomic (+) strand synthesis. However, the promoters of (+) strand genomic RNA synthesis are as yet undefined. In vivo viral RNA synthesis is usually highly asymmetric with many times more (+) strand RNA being synthesized than (-) strand.n tRNA gene transcription in eukaryotes, dependent on polymerase III and associated transcription factors, is a nuclear process. The apparent homology to promoters of tRNAs suggests involvement of host factors in viral (+) strand synthesis, possibly pol III transcription factors are proposed. Experiments are to define which elements within and surrounding the ICRs of BMV are essential and functional in replication. Furthermore, the role of the ICRs in the asymmetry of replication, and in determining the specific molar ratios of genomic RNAs synthesized is addressed. Identification of the host factor(s) involved in replication is essential in that they are the core of the host-pathogen relationship.