Ansardi D C, Porter D C, Morrow C D
Department of Microbiology, University of Alabama 35294-0007.
J Virol. 1993 Jun;67(6):3684-90. doi: 10.1128/JVI.67.6.3684-3690.1993.
Defective interfering (DI) RNA genomes of poliovirus which contain in-frame deletions in the P1 capsid protein-encoding region have been described. DI genomes are capable of replication and can be encapsidated by capsid proteins provided in trans from wild-type poliovirus. In this report, we demonstrate that a previously described poliovirus DI genome (K. Hagino-Yamagishi and A. Nomoto, J. Virol. 63:5386-5392, 1989) can be complemented by a recombinant vaccinia virus, VVP1 (D. C. Ansardi, D. C. Porter, and C. D. Morrow, J. Virol. 65:2088-2092, 1991), which expresses the poliovirus capsid precursor polyprotein, P1. Stocks of defective polioviruses were generated by transfecting in vitro-transcribed defective genome RNA derived from plasmid pSM1(T7)1 into HeLa cells infected with VVP1 and were maintained by serial passage in the presence of VVP1. Encapsidation of the defective poliovirus genome was demonstrated by characterizing poliovirus-specific protein expression in cells infected with preparations of defective poliovirus and by Northern (RNA) blot analysis of poliovirus-specific RNA incorporated into defective poliovirus particles. Cells infected with preparations of defective poliovirus expressed poliovirus protein 3CD but did not express capsid proteins derived from a full-length P1 precursor. Poliovirus-specific RNA encapsidated in viral particles generated in cells coinfected with VVP1 and defective poliovirus migrated slightly faster on formaldehyde-agarose gels than wild-type poliovirus RNA, demonstrating maintenance of the genomic deletion. By metabolic radiolabeling with [35S]methionine-cysteine, the defective poliovirus particles were shown to contain appropriate mature-virion proteins. This is the first report of the generation of a pure population of defective polioviruses free of contaminating wild-type poliovirus. We demonstrate the use of this recombinant vaccinia virus-defective poliovirus genome complementation system for studying the effects of a defined mutation in the P1 capsid precursor on virus assembly. Following removal of residual VVP1 from defective poliovirus preparations, processing and assembly of poliovirus capsid proteins derived from a nonmyristylated P1 precursor expressed by a recombinant vaccinia virus, VVP1 myr- (D. C. Ansardi, D. C. Porter, and C. D. Morrow, J. Virol. 66:4556-4563, 1992), in cells coinfected with defective poliovirus were analyzed. Capsid proteins generated from nonmyristylated P1 did not assemble detectable levels of mature virions but did assemble, at low levels, into empty capsids.(ABSTRACT TRUNCATED AT 400 WORDS)
已描述了脊髓灰质炎病毒的缺陷干扰(DI)RNA基因组,其在P1衣壳蛋白编码区含有读框内缺失。DI基因组能够复制,并且可以被野生型脊髓灰质炎病毒反式提供的衣壳蛋白包裹。在本报告中,我们证明了一种先前描述的脊髓灰质炎病毒DI基因组(K. Hagino - Yamagishi和A. Nomoto,《病毒学杂志》63:5386 - 5392,1989年)可以被重组痘苗病毒VVP1(D. C. Ansardi、D. C. Porter和C. D. Morrow,《病毒学杂志》65:2088 - 2092,1991年)互补,该重组痘苗病毒表达脊髓灰质炎病毒衣壳前体多蛋白P1。通过将源自质粒pSM1(T7)1的体外转录缺陷基因组RNA转染到感染VVP1的HeLa细胞中,产生了缺陷脊髓灰质炎病毒毒株,并在VVP1存在下通过连续传代进行维持。通过表征感染缺陷脊髓灰质炎病毒制剂的细胞中脊髓灰质炎病毒特异性蛋白表达以及对掺入缺陷脊髓灰质炎病毒颗粒中的脊髓灰质炎病毒特异性RNA进行Northern(RNA)印迹分析,证明了缺陷脊髓灰质炎病毒基因组的衣壳化。感染缺陷脊髓灰质炎病毒制剂的细胞表达脊髓灰质炎病毒蛋白3CD,但不表达源自全长P1前体的衣壳蛋白。在与VVP1和缺陷脊髓灰质炎病毒共感染的细胞中产生的病毒颗粒中包裹的脊髓灰质炎病毒特异性RNA在甲醛 - 琼脂糖凝胶上的迁移速度比野生型脊髓灰质炎病毒RNA略快,这表明基因组缺失得以维持。通过用[35S]甲硫氨酸 - 半胱氨酸进行代谢放射性标记,显示缺陷脊髓灰质炎病毒颗粒含有适当的成熟病毒粒子蛋白。这是关于产生不含野生型脊髓灰质炎病毒污染的纯缺陷脊髓灰质炎病毒群体的首次报告。我们展示了这种重组痘苗病毒 - 缺陷脊髓灰质炎病毒基因组互补系统用于研究P1衣壳前体中特定突变对病毒装配的影响。在从缺陷脊髓灰质炎病毒制剂中去除残留的VVP1后,分析了由重组痘苗病毒VVP1 myr - (D. C. Ansardi、D. C. Porter和C. D. Morrow,《病毒学杂志》66:4556 - 4563,1992年)表达的非肉豆蔻酰化P1前体衍生的脊髓灰质炎病毒衣壳蛋白在与缺陷脊髓灰质炎病毒共感染的细胞中的加工和装配情况。由非肉豆蔻酰化P1产生的衣壳蛋白没有装配成可检测水平的成熟病毒粒子,但确实以低水平装配成了空衣壳。(摘要截断于400字)