Aranda M A, Escaler M, Wang D, Maule A J
Department of Virus Research, John Innes Centre, Colney, Norwich, United Kingdom.
Proc Natl Acad Sci U S A. 1996 Dec 24;93(26):15289-93. doi: 10.1073/pnas.93.26.15289.
By examining the front of virus invasion in immature pea embryos infected with pea seed-borne mosaic virus (PSbMV), the selective control of different host genes has been observed. From our observations, the early responses to PSbMV replication can be grouped into three classes, inhibited host gene expression, induced host gene expression, and no effect on a normal host function. The expression of two heat-inducible genes encoding HSP70 and polyubiquitin was induced coordinately with the onset of virus replication and the down-regulation of two other genes encoding lipoxygenase and heat shock cognate protein. The down-regulation was part of a general suppression of host gene expression that may be achieved through the degradation of host transcripts. We discuss the possibilities of whether the induction of HSP70 and polyubiquitin genes represents a requirement for the respective protein products by the virus or is merely a consequence of the depletion of other host transcripts. The former is feasible, as the induction of both genes does result in increased HSP70 and ubiquitin accumulation. This also indicates that, in contrast to some animal virus infections, there is not a general inhibition of translation of host mRNAs following PSbMV infection. This selective control of host gene expression was observed in all cell types of the embryo and identifies mechanisms of cellular disruption that could act as triggers for symptom expression.
通过检查感染豌豆种传花叶病毒（PSbMV）的未成熟豌豆胚中病毒入侵的前沿，观察到了不同宿主基因的选择性调控。根据我们的观察，对PSbMV复制的早期反应可分为三类：宿主基因表达受抑制、宿主基因表达被诱导以及对正常宿主功能无影响。两个编码HSP70和多聚泛素的热诱导基因的表达与病毒复制的开始以及另外两个编码脂氧合酶和热休克同源蛋白的基因的下调协同诱导。这种下调是宿主基因表达普遍抑制的一部分，可能是通过宿主转录本的降解实现的。我们讨论了HSP70和多聚泛素基因的诱导是病毒对相应蛋白质产物的需求，还是仅仅是其他宿主转录本耗竭的结果。前者是可行的，因为这两个基因的诱导确实导致了HSP70和泛素积累的增加。这也表明，与一些动物病毒感染不同，PSbMV感染后宿主mRNA的翻译并没有普遍受到抑制。在胚的所有细胞类型中都观察到了这种对宿主基因表达的选择性调控，并且确定了可能作为症状表达触发因素的细胞破坏机制。
