Stow N D
Medical Research Council Virology Unit, Institute of Virology, Glasgow, U.K.
J Gen Virol. 1992 Feb;73 ( Pt 2):313-21. doi: 10.1099/0022-1317-73-2-313.
The minimal set of seven herpes simplex virus type 1 (HSV-1) genes required for viral origin-dependent DNA synthesis was previously identified using a transient replication assay in a mammalian cell line permissive for HSV-1 growth. We have constructed recombinant baculoviruses which efficiently express the products of each of these seven genes in infected Spodoptera frugiperda (Sf) insect cells. When Sf cells were transfected with a plasmid containing a functional HSV-1 origin of replication, and subsequently superinfected with a mixture of these seven viruses, the input plasmid was amplified. This amplification exhibited properties characteristic of genuine HSV-1 DNA replication: all seven HSV-1 replication gene products were required, replicated DNA was detected as concatemers, and mutated origins were impaired to similar extents in insect cells and cells permissive for HSV-1 replication. These results demonstrate that the HSV-1 proteins expressed in Sf cells are fully competent for viral DNA synthesis, and indicate that any host function essential in mammalian cells must also be present in the infected insect cells. This system also provides a convenient method by which mutated replication proteins can be screened for function and produced in amounts sufficient for biochemical studies. Using this approach we show that the ability of the UL9 protein to bind to the viral origins of replication is not sufficient for it to facilitate DNA synthesis.
先前利用对单纯疱疹病毒1型(HSV-1)生长具有允许性的哺乳动物细胞系中的瞬时复制分析,鉴定出了病毒起始依赖型DNA合成所需的最少7个HSV-1基因。我们构建了重组杆状病毒,其能在被感染的草地贪夜蛾(Sf)昆虫细胞中高效表达这7个基因中每个基因的产物。当用含有功能性HSV-1复制起点的质粒转染Sf细胞,随后用这7种病毒的混合物进行超感染时,输入的质粒得到了扩增。这种扩增表现出真正的HSV-1 DNA复制的特征:所有7种HSV-1复制基因产物都是必需的,复制的DNA被检测为多联体,并且在昆虫细胞和对HSV-1复制具有允许性的细胞中,突变的起点受到的损害程度相似。这些结果表明,在Sf细胞中表达的HSV-1蛋白完全具备病毒DNA合成的能力,并表明在哺乳动物细胞中必需的任何宿主功能在被感染的昆虫细胞中也必定存在。该系统还提供了一种便捷的方法,通过此方法可以筛选突变的复制蛋白的功能,并产生足以用于生化研究的量。利用这种方法,我们表明UL9蛋白与病毒复制起点结合的能力不足以促进DNA合成。