Wilcock D, Smith G L
Sir William Dunn School of Pathology, University of Oxford, United Kingdom.
Virology. 1994 Jul;202(1):294-304. doi: 10.1006/viro.1994.1346.
A recombinant vaccinia virus, vDW4, has been constructed in which the L4R gene encoding the VP8 core DNA-binding protein is inducibly regulated by IPTG (isopropyl beta-D-thiogalactopyranoside). This virus produced normal-sized plaques in the presence of IPTG, but tiny plaques in the absence of inducer. Production of infectious progeny virus was reduced by 97% when VP8 synthesis was repressed and immature virions which had defective interactions between the granular viroplasm and the surrounding virion membrane were evident. However, despite the formation of these abnormal immature virions, virus maturation was able to proceed with the production of mature intracellular naked virus and extracellular enveloped virus particles of normal density. These mature particles were produced to approximately 80% of wild-type levels, but were around 100-fold less infectious. Consistent with the formation of mature virions, the repression of VP8 synthesis did not inhibit proteolytic processing of the major core proteins p4a and p4b. These results suggest that VP8 is required for correct association of the viroplasm and the immature virion envelope and that VP8 must be present during virus assembly for the production of fully infectious progeny virus.
构建了一种重组痘苗病毒vDW4,其中编码VP8核心DNA结合蛋白的L4R基因受IPTG(异丙基-β-D-硫代半乳糖苷)诱导调控。该病毒在IPTG存在下产生正常大小的噬斑,但在没有诱导剂的情况下产生微小噬斑。当VP8合成受到抑制时,感染性子代病毒的产生减少了97%,并且明显可见颗粒状病毒质与周围病毒体膜之间相互作用存在缺陷的未成熟病毒体。然而,尽管形成了这些异常的未成熟病毒体,病毒成熟仍能够进行,产生成熟的细胞内裸病毒和正常密度的细胞外包膜病毒颗粒。这些成熟颗粒的产量约为野生型水平的80%,但感染性约低100倍。与成熟病毒体的形成一致,VP8合成的抑制并未抑制主要核心蛋白p4a和p4b的蛋白水解加工。这些结果表明,VP8是病毒质与未成熟病毒体包膜正确结合所必需的,并且在病毒组装过程中必须存在VP8才能产生完全感染性的子代病毒。