Frígols Belén, Quiles-Puchalt Nuria, Mir-Sanchis Ignacio, Donderis Jorge, Elena Santiago F, Buckling Angus, Novick Richard P, Marina Alberto, Penadés José R
Universidad Cardenal Herrera CEU, Moncada, Spain.
Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
PLoS Genet. 2015 Oct 23;11(10):e1005609. doi: 10.1371/journal.pgen.1005609. eCollection 2015 Oct.
Virus satellites are widespread subcellular entities, present both in eukaryotic and in prokaryotic cells. Their modus vivendi involves parasitism of the life cycle of their inducing helper viruses, which assures their transmission to a new host. However, the evolutionary and ecological implications of satellites on helper viruses remain unclear. Here, using staphylococcal pathogenicity islands (SaPIs) as a model of virus satellites, we experimentally show that helper viruses rapidly evolve resistance to their virus satellites, preventing SaPI proliferation, and SaPIs in turn can readily evolve to overcome phage resistance. Genomic analyses of both these experimentally evolved strains as well as naturally occurring bacteriophages suggest that the SaPIs drive the coexistence of multiple alleles of the phage-coded SaPI inducing genes, as well as sometimes selecting for the absence of the SaPI depressing genes. We report similar (accidental) evolution of resistance to SaPIs in laboratory phages used for Staphylococcus aureus typing and also obtain the same qualitative results in both experimental evolution and phylogenetic studies of Enterococcus faecalis phages and their satellites viruses. In summary, our results suggest that helper and satellite viruses undergo rapid coevolution, which is likely to play a key role in the evolution and ecology of the viruses as well as their prokaryotic hosts.
病毒卫星是广泛存在的亚细胞实体,存在于真核细胞和原核细胞中。它们的生存方式涉及寄生在其诱导辅助病毒的生命周期中,这确保了它们传播到新的宿主。然而,卫星对辅助病毒的进化和生态影响仍不清楚。在这里,我们以葡萄球菌致病岛(SaPIs)作为病毒卫星的模型,通过实验表明辅助病毒会迅速进化出对其病毒卫星的抗性,从而阻止SaPI的增殖,而SaPIs反过来又能很容易地进化以克服噬菌体抗性。对这些实验进化菌株以及天然存在的噬菌体的基因组分析表明,SaPIs推动了噬菌体编码的SaPI诱导基因多个等位基因的共存,有时还会选择不存在SaPI抑制基因的情况。我们报告了用于金黄色葡萄球菌分型的实验室噬菌体中对SaPIs的类似(偶然)抗性进化,并且在粪肠球菌噬菌体及其卫星病毒的实验进化和系统发育研究中也得到了相同的定性结果。总之,我们的结果表明辅助病毒和卫星病毒经历了快速的协同进化,这可能在病毒及其原核宿主的进化和生态中发挥关键作用。