The evolution of small DNA viruses of eukaryotes: past and present considerations.
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.
Shadan
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Department of Molecular Biology and Biochemistry, University of California, Irvine 92717, USA.
Villarreal
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D000222:Adaptation, Physiological / Q000276:immunology; D000818:Animals; D016207:Cytokines / Q000276:immunology; D004267:DNA Viruses / Q000235:genetics* / Q000276:immunology*; D005057:Eukaryotic Cells / Q000276:immunology; D019143:Evolution, Molecular; D006801:Humans; D007107:Immune System / Q000276:immunology; D007109:Immunity; D010802:Phylogeny; D012641:Selection, Genetic; D014714:Vertebrates / Q000276:immunology / Q000821:virology
D016207:Cytokines