Shadan F F, Villarreal L P
Department of Molecular Biology and Biochemistry, University of California, Irvine 92717, USA.
Virus Genes. 1995;11(2-3):239-57. doi: 10.1007/BF01728663.
Historically, viral evolution has often been considered from the perspective of the ability of the virus to maintain viral pathogenic fitness by causing disease. A predator-prey model has been successfully applied to explain genetically variable quasi-species of viruses, such as influenza virus and human immunodeficiency virus (HIV), which evolve much faster rates than the host. In contrast, small DNA viruses (polyomaviruses, papillomaviruses, and parvoviruses) are species specific but are stable genetically, and appear to have co-evolved with their host species. Genetic stability is attributable primarily to the ability to establish and maintain a benign persistent state in vivo and not to the host DNA proofreading mechanisms. The persistent state often involves a cell cycle-regulated episomal state and a tight linkage of DNA amplification mechanisms to cellular differentiation. This linkage requires conserved features among viral regulatory proteins, with characteristic host-interactive domains needed to recruit and utilize host machinery, thus imposing mechanistic constrains on possible evolutionary options. Sequence similarities within these domains are seen amongst all small mammalian DNA viruses and most of the parvo-like viruses, including those that span the entire spectrum of evolution of organisms from E. coli to humans that replicate via a rolling circle-like mechanism among the entire spectrum of organisms throughout evolution from E. coli to humans. To achieve benign inapparent viral persistence, small DNA viruses are proposed to circumvent the host acute phase reaction (characterized by minimal inflammation) by mechanisms that are evolutionarily adapted to the immune system and the related cytokine communication networks. A striking example of this is the relationship of hymenoptera to polydnaviruses, in which the crucial to the recognition of self, development, and maintenance of genetic identity of both the host and virus. These observations in aggregate suggest that viral replicons are not recent "escapies" of host replication, but rather provide relentless pressure in driving the evolution of the host through cospeciation.
从历史上看，病毒进化通常是从病毒通过引发疾病来维持病毒致病适应性的能力这一角度来考虑的。一种捕食者 - 猎物模型已成功应用于解释病毒的基因可变准种，如流感病毒和人类免疫缺陷病毒（HIV），它们的进化速度比宿主快得多。相比之下，小型DNA病毒（多瘤病毒、乳头瘤病毒和细小病毒）具有物种特异性，但基因稳定，并且似乎与它们的宿主物种共同进化。遗传稳定性主要归因于在体内建立和维持良性持续状态的能力，而非宿主DNA校对机制。这种持续状态通常涉及细胞周期调控的附加体状态以及DNA扩增机制与细胞分化的紧密联系。这种联系需要病毒调节蛋白之间具有保守特征，以及具有特征性的宿主相互作用结构域来招募和利用宿主机制，从而对可能的进化选择施加机制限制。在所有小型哺乳动物DNA病毒和大多数细小病毒样病毒中都能看到这些结构域内的序列相似性，包括那些跨越从大肠杆菌到人类整个生物进化谱、通过滚环样机制在整个进化过程中从大肠杆菌到人类的所有生物中进行复制的病毒。为了实现良性无症状的病毒持续感染，小型DNA病毒被认为是通过在进化上适应免疫系统和相关细胞因子通讯网络的机制来规避宿主急性期反应（以最小炎症为特征）。一个显著的例子是膜翅目昆虫与多分DNA病毒的关系，其中对于宿主和病毒的自我识别、发育以及遗传身份的维持至关重要。这些总体观察结果表明，病毒复制子并非宿主复制的近期“逃逸者”，而是通过共同物种形成在推动宿主进化过程中提供了持续的压力。
