THE 3'-NUCLEOTIDES OF FLAVIVIRUS GENOMIC RNA FORM A CONSERVED SECONDARY STRUCTURE
THE 3'-NUCLEOTIDES OF FLAVIVIRUS GENOMIC RNA FORM A CONSERVED SECONDARY STRUCTURE
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DOI：
10.1016/0042-6822(86)90012-7
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发表时间：
1986-08-01
期刊：
影响因子：
3.7
通讯作者：
DISPOTO, JH
中科院分区：
文献类型：
--
作者：
BRINTON, MA;FERNANDEZ, AV;DISPOTO, JH
据推测，病毒 RNA 基因组的末端非编码区含有信号序列，有时还含有参与调节病毒 RNA 合成的二级结构。预计此类信号在相关病毒中高度保守。为了确定黄病毒的复制信号特征，我们比较了西尼罗河病毒 (WNV)、圣路易斯脑炎 (SLE) 病毒和黄热病病毒 (YFV) 基因组 RNA 的 3'' 末端核苷酸序列。先前通过从 YFV 基因组 RNA 获得的 cDNA 序列预测了稳定的 3'' 末端二级结构的存在。我们通过直接RNA测序方法证实了这种结构的存在。尽管 3'' 末端二级结构的大小和形状高度保守，但序列保守性仅限于二级结构的环区域和紧邻该结构 5'' 侧的 27 个核苷酸。保守序列区域代表了病毒聚合酶识别和结合的可能信号。然而，通过序列保存以外的方式保存二级结构的构型表明该结构对于病毒的生存很重要。一种 WNV 突变体比亲本 WNV 更有效地复制子代基因组 RNA，被发现具有与其亲本病毒相同的 3'' 基因组序列。因此，赋予该突变体表型的序列变化位于基因组的另一个区域。
The terminal noncoding regions of viral RNA genomes are presumed to contain signal sequences and sometimes also secondary structures involved in regulating viral RNA synthesis. Such signals would be expected to be highly conserved among related viruses. In order to identify replication signal features for flaviviruses we have compared the 3''-terminal nucleotide sequences of West Nile virus (WNV), Saint Louis encephalitis (SLE) virus, and yellow fever virus (YFV) genome RNAs. The existence of a stable 3''-terminal secondary structure was previously predicted by a cDNA sequence obtained from YFV genome RNA. We have confirmed the existence of this structure by direct RNA sequencing methods. Even though the size and shape of the 3''-terminal secondary structure is highly conserved, sequence conservation is restricted to the loop regions of the secondary structure and to 27 nucleotides immediately adjacent to the 5'' side of the structure. The regions of conserved sequence represent likely signals for viral polymerase recognition and binding. However, the preservation of the configuration of the secondary structure by a means other than sequence conservation indicate that this structure is important for the survival of the virus. A WNV mutant, which replicates progeny genome RNA more efficiently than parental WNV, was found to have a 3''-genomic sequence identical to that of its parent virus. The sequence change conferring the phenotype of this mutant is therefore located in another region of the genome.