Wilcock D, Smith G L
Sir William Dunn School of Pathology, University of Oxford, United Kingdom.
J Virol. 1996 Feb;70(2):934-43. doi: 10.1128/JVI.70.2.934-943.1996.
When synthesis of the 25-kDa vaccinia virus core protein VP8 is repressed, mature virus particles of normal appearance are produced to approximately 80% of wild-type levels but these particles are over 100-fold less infectious than wild-type particles (D. Wilcock and G. L. Smith, Virology 202:294-304, 1994). Here we show that virions which lack VP8 can bind to and enter cells but the levels of steady-state RNA are greatly reduced in comparison with those for wild-type infections. In vitro assays using permeabilized virions demonstrated that VP8-deficient virions had drastically reduced rates of transcription (RNA synthesis was decreased by 80 to 96%) and that the extrusion of RNA transcripts from these virions was also decreased. Low concentrations of sodium deoxycholate extracted proteins more efficiently from VP8-deficient virions than from wild-type virions. The increased fragility of VP8-deficient virions and their slower RNA extrusion rates suggest that VP8 may be required for the correct formation of the core. Virions which lack VP8 were shown to contain a full complement of transcription enzymes, and soluble extracts from these virions were active in transcription assays using either single-stranded M13 DNA or exogenous plasmid template containing a vaccinia virus early promoter. Thus, the defect in transcription is due not to a lack of specific transcriptional enzymes within virions but rather to the inability of these enzymes to efficiently transcribe the DNA genome packaged within VP8-deficient virions. These results suggest that VP8 is required for the correct packaging of the viral DNA genome and/or for the efficient transcription of packaged virion DNA, which has a higher degree of structural complexity than plasmid templates. Possible roles for VP8 in these processes are discussed.
当25 kDa痘苗病毒核心蛋白VP8的合成受到抑制时,会产生外观正常的成熟病毒颗粒,其数量约为野生型水平的80%,但这些颗粒的感染性比野生型颗粒低100倍以上(D. 威尔科克和G. L. 史密斯,《病毒学》202:294 - 304,1994年)。在此我们表明,缺乏VP8的病毒粒子能够结合并进入细胞,但与野生型感染相比,稳态RNA水平大幅降低。使用透化病毒粒子的体外试验表明,缺乏VP8的病毒粒子转录速率大幅降低(RNA合成减少80%至96%),并且这些病毒粒子中RNA转录本的挤出也减少。低浓度的脱氧胆酸钠从缺乏VP8的病毒粒子中提取蛋白质比从野生型病毒粒子中更有效。缺乏VP8的病毒粒子增加的脆弱性及其较慢的RNA挤出速率表明,VP8可能是核心正确形成所必需的。已证明缺乏VP8的病毒粒子含有完整的转录酶补充,并且这些病毒粒子的可溶性提取物在使用单链M13 DNA或含有痘苗病毒早期启动子的外源质粒模板的转录试验中具有活性。因此,转录缺陷不是由于病毒粒子内缺乏特定的转录酶,而是由于这些酶无法有效转录包装在缺乏VP8的病毒粒子内的DNA基因组。这些结果表明,VP8是病毒DNA基因组正确包装和/或包装的病毒粒子DNA有效转录所必需的,病毒粒子DNA的结构复杂性高于质粒模板。本文讨论了VP8在这些过程中的可能作用。