Doyle M, Holland J J
J Virol. 1972 Jan;9(1):22-8. doi: 10.1128/JVI.9.1.22-28.1972.
In doubly infected HeLa cells, poliovirus type 1 rapidly and completely dominates vesicular stomatitis virus (VSV) plaque-forming unit production. Poliovirus type 1 shuts off incorporation of amino acids into VSV-specific proteins within 2 hr after superinfection of cells already committed to massive synthesis of VSV proteins. However, poliovirus type 1 appears to have little, if any, direct effect upon incorporation of uridine into VSV-directed ribonucleic acid (RNA) synthesis. Poliovirus apparently interferes with VSV virion production only at the level of translation of viral messenger RNA, although it interferes with host cell macromolecular syntheses at the levels of translation and transcription.
在双重感染的HeLa细胞中,1型脊髓灰质炎病毒迅速且完全主导水泡性口炎病毒(VSV)空斑形成单位的产生。在已经致力于大量合成VSV蛋白的细胞再次感染后2小时内,1型脊髓灰质炎病毒就会阻止氨基酸掺入VSV特异性蛋白中。然而,1型脊髓灰质炎病毒似乎对尿苷掺入VSV指导的核糖核酸(RNA)合成几乎没有直接影响,即使有影响也很小。脊髓灰质炎病毒显然仅在病毒信使RNA的翻译水平上干扰VSV病毒粒子的产生,尽管它在翻译和转录水平上干扰宿主细胞的大分子合成。