Complete nucleotide sequence of chikungunya virus and evidence for an internal polyadenylation site
Complete nucleotide sequence of chikungunya virus and evidence for an internal polyadenylation site
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DOI：
10.1099/0022-1317-83-12-3075
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发表时间：
2002-12-01
影响因子：
3.8
通讯作者：
Igarashi, A
中科院分区：
文献类型：
--
作者：
Khan, AH;Morita, K;Igarashi, A
本研究测定了基孔肯雅病毒（CHIK; S27 African prototype）的全基因组序列，并证实了该毒株3'非翻译区（NTR）内存在内部多聚腺苷酸化[l-poly（A）]位点。该基因组全长11805个核苷酸，不包括5'端帽核苷酸、1个I-poly（A）区和3'端poly（A）尾。它包含两个长的开放阅读框架，编码非结构性多聚蛋白（2474个氨基酸）和结构性多聚蛋白（1244个氨基酸）。通过比较推导的氨基酸序列与其他甲病毒的已知切割位点（位于其病毒编码蛋白的C-末端区域），预测非结构蛋白和结构蛋白的遗传位置。此外，在5' NTR内鉴定了预测的二级结构，并在3' NTR内鉴定了重复序列元件（RSE）。氨基酸序列同源性、非结构蛋白和结构蛋白的系统发育分析以及特征性RSE显示，尽管CHIK与o 'nyong-nyong病毒密切相关，但它实际上是一种不同的病毒。在每个克隆的相同起始位置存在不同长度（例如19、36、43、91、94和106个腺嘌呤核苷酸）的I-poly（A）片段，这强烈地表明甲病毒的聚合酶具有通过模板依赖性机制（例如I聚合酶滑动）产生poly（A）的能力，如对于水泡性口炎病毒所报道的。
In this study, the complete genomic sequence of chikungunya virus (CHIK; S27 African prototype) was determined and the presence of an internal polyadenylation [l-poly(A)] site was confirmed within the 3' non-translated region (NTR) of this strain. The complete genome was 11805 nucleotides in length, excluding the 5' cap nucleotide, an I-poly(A) tract and the 3' poly(A) tail. It comprised two long open reading frames that encoded the non-structural (2474 amino acids) and structural polyproteins (1244 amino acids). The genetic location of the non-structural and structural proteins was predicted by comparing the deduced amino acid sequences with the known cleavage sites of other alphaviruses, located at the C-terminal region of their virus-encoded proteins. In addition, predicted secondary structures were identified within the 5' NTR and repeated sequence elements (RSEs) within the 3' NTR. Amino acid sequence homologies, phylogenetic analysis of non-structural and structural proteins and characteristic RSEs revealed that although CHIK is closely related to o'nyong-nyong virus, it is in fact a distinct virus. The existence of I-poly(A) fragments with different lengths (e.g. 19, 36, 43, 91, 94 and 106 adenine nucleotides) at identical initiation positions for each clone strongly suggests that the polymerase of the alphaviruses has a capacity to create poly(A) by a template-dependant mechanism such as I polymerase slippage', as has been reported for vesicular stomatitis virus.