Abstract：
The entry of a virus into the host cell always implies the alteration of certain intracellular molecular relationships, some of which may involve the recovery of ancient cellular activities. In this sense, viruses are archaeological tools for identifying unexpressed activities in noninfected cells. Among these, activities that hinder virus propagation may represent cellular defense mechanisms, for example, activities that mutagenize the viral genome such as ADAR-1 or APOBEC activities. Instead, those that facilitate virus propagation can be interpreted as the result of viral adaptation to-or mimicking-cellular structures, enabling the virus to perform anthropomorphic activities, including hijacking, manipulating, and reorganizing cellular factors for their own benefit. The alternative we consider here is that some of these second set of cellular activities were already in the uninfected cell but silenced, under the negative control of the cell or lineage, and that they represent a necessary precondition for viral infection. For example, specifically loading an amino acid at the 3\'-end of the mRNA of some plant viruses by aminoacyl-tRNA synthetases has proved essential for virus infection despite this reaction not occurring with cellular mRNAs. Other activities of this type are discussed here, together with the biological context in which they acquire a coherent meaning, that is, genetic latency and molecular conflict.
摘要：
病毒进入宿主细胞总是意味着某些细胞内分子关系的改变，其中一些可能涉及古代细胞活动的恢复。在这个意义上,病毒是用于识别未感染细胞中未表达活性的考古工具。其中,阻碍病毒传播的活动可能代表细胞防御机制，例如,突变病毒基因组的活性，如ADAR-1或APOBEC活性。相反，那些促进病毒繁殖的可以解释为病毒适应或模仿细胞结构的结果，使病毒能够进行拟人化活动，包括劫持,操纵，操纵和重组细胞因子为自己的利益。我们在这里考虑的另一种选择是，这些第二组细胞活动中的一些已经在未感染的细胞中，但被沉默了，在细胞或谱系的阴性控制下，它们是病毒感染的必要先决条件。例如,通过氨酰基-tRNA合成酶在某些植物病毒mRNA的3'末端特异性加载氨基酸已被证明对病毒感染至关重要，尽管这种反应不会发生在细胞mRNA上。其他此类活动在此讨论，以及它们获得连贯含义的生物学背景，也就是说,遗传潜伏期和分子冲突。
