Kääriäinen L, Takkinen K, Keränen S, Söderlund H
Recombinant DNA Laboratory, University of Helsinki, Finland.
J Cell Sci Suppl. 1987;7:231-50.
The genome of Semliki Forest virus (SFV) is 11,442 nucleotides with a 5' cap-structure and a 3' poly(A) tail of about 100 residues. The genome of the closely relate Sindbis virus (SIN) is slightly longer (11,703 nucleotides). The parental RNA is first translated from the 5' two thirds to yield; nsP1, nsP2, nsP3 and nsP4, which are cleaved from a polyprotein of 2431 amino acids (SFV). The parental genome is copied to a full-length minus strand with poly(U) at the 5' end. The minus strand is used as template for the synthesis of 42 S RNA in membrane-bound replicative-intermediate (RI) structures. In addition to 42 S RNA, a 3'-coterminal subgenomic 26 S mRNA, coding for the structural proteins, is synthesized by internal initiation at the minus strand. Capping and methylation of both plus-strand RNAs occur concomitantly with their synthesis. Analysis of Sindbis virus temperature-sensitive RNA-negative mutants have shown that one complementation group (B) is specifically associated with the synthesis of minus strands. Another, group F, is involved in the polymerization step of both minus- and plus-strand 42 S RNA, and of the 26 S mRNA. The synthesis of minus strands is normally dependent on protein synthesis. There is a shut off of the minus-strand RNA synthesis at about 3 h post-infection. This is apparently regulated by a virus-specific protein, represented by the complementation group A. The same protein is involved in the regulation of the initiation of 26 S RNA together with a component represented by group G mutants. Comparative analysis of SFV and SIN RNAs and DI RNAs of both viruses suggests that perhaps only 19 nucleotides from the 3' end and about 150 nucleotides from the 5' end are needed for replication of the alphavirus RNAs. In some SIN DI RNAs the proposed secondary structure at the 5' end is replaced by a cellular tRNA(ASP) suggesting that the secondary structure rather than nucleotide sequence is sufficient for the recognition by the viral polymerase. Even when the primary structure of the four non-structural proteins of both SFV and SIN is known, the correlation of the genetic data with the individual proteins has not yet been possible.
辛德毕斯病毒（Semliki Forest virus，SFV）的基因组有11442个核苷酸，带有5'帽结构和一个约100个残基的3'多聚腺苷酸尾。密切相关的辛德毕斯病毒（Sindbis virus，SIN）的基因组稍长（11703个核苷酸）。亲代RNA首先从5'端的三分之二处开始翻译，产生nsP1、nsP2、nsP3和nsP4，它们是从一个2431个氨基酸的多聚蛋白（SFV）上切割下来的。亲代基因组被复制成一条5'端带有聚（U）的全长负链。负链被用作模板，在膜结合的复制中间体（RI）结构中合成42S RNA。除了42S RNA外，还通过在负链上的内部起始合成一条编码结构蛋白的3'共末端亚基因组26S mRNA。正链RNA的加帽和甲基化与它们的合成同时发生。对辛德毕斯病毒温度敏感RNA阴性突变体的分析表明，一个互补组（B）与负链的合成特异性相关。另一个F组则参与负链和正链42S RNA以及26S mRNA的聚合步骤。负链的合成通常依赖于蛋白质合成。在感染后约3小时，负链RNA合成会停止。这显然是由一个病毒特异性蛋白调控的，该蛋白由互补组A代表。同一蛋白与G组突变体代表的一个成分一起参与26S RNA起始的调控。对SFV和SIN的RNA以及两种病毒的缺陷干扰RNA（DI RNA）的比较分析表明，对于甲病毒RNA的复制，可能仅需要3'端的19个核苷酸和约5'端的150个核苷酸。在一些SIN DI RNA中，5'端提议的二级结构被一个细胞tRNA（ASP）取代，这表明二级结构而非核苷酸序列对于病毒聚合酶的识别就足够了。即使已经知道了SFV和SIN的四种非结构蛋白的一级结构，遗传数据与各个蛋白之间的关联仍未实现。
