Department of Microbiology, University of Illinois, Urbana-Champaign, Urbana, Illinois, USA.
Department of Microbiology, University of Illinois, Urbana-Champaign, Urbana, Illinois, USA
mBio. 2020 Apr 28;11(2):e00404-20. doi: 10.1128/mBio.00404-20.
Theory, simulation, and experimental evolution demonstrate that diversified CRISPR-Cas immunity to lytic viruses can lead to stochastic virus extinction due to a limited number of susceptible hosts available to each potential new protospacer escape mutation. Under such conditions, theory predicts that to evade extinction, viruses evolve toward decreased virulence and promote vertical transmission and persistence in infected hosts. To better understand the evolution of host-virus interactions in microbial populations with active CRISPR-Cas immunity, we studied the interaction between CRISPR-immune cells and immune-deficient strains that are infected by the chronic virus SSV9. We demonstrate that cells infected with SSV9, and with other related SSVs, kill uninfected, immune strains through an antagonistic mechanism that is a protein and is independent of infectious virus. Cells that are infected with SSV9 are protected from killing and persist in the population. We hypothesize that this infection acts as a form of mutualism between the host and the virus by removing competitors in the population and ensuring continued vertical transmission of the virus within populations with diversified CRISPR-Cas immunity. Multiple studies, especially those focusing on the role of lytic viruses in key model systems, have shown the importance of viruses in shaping microbial populations. However, it has become increasingly clear that viruses with a long host-virus interaction, such as those with a chronic lifestyle, can be important drivers of evolution and have large impacts on host ecology. In this work, we describe one such interaction with the acidic crenarchaeon and its chronic virus spindle-shaped virus 9. Our work expands the view in which this symbiosis between host and virus evolved, describing a killing phenotype which we hypothesize has evolved in part due to the high prevalence and diversity of CRISPR-Cas immunity seen in natural populations. We explore the implications of this phenotype in population dynamics and host ecology, as well as the implications of mutualism between this virus-host pair.
理论、模拟和实验进化表明，多样化的 CRISPR-Cas 免疫对裂解病毒可能导致随机病毒灭绝，因为每个潜在的新间隔区逃逸突变都只有有限数量的易感宿主。在这种情况下，理论预测为了避免灭绝，病毒会朝着降低毒力的方向进化，并促进受感染宿主中的垂直传播和持久性。为了更好地理解具有活跃 CRISPR-Cas 免疫的微生物种群中宿主-病毒相互作用的进化，我们研究了 CRISPR 免疫细胞与免疫缺陷株之间的相互作用，这些免疫缺陷株被慢性病毒 SSV9 感染。我们证明，感染了 SSV9 以及其他相关 SSV 的细胞通过一种拮抗机制杀死未感染的免疫株，这种机制是一种独立于传染性病毒的蛋白质。感染了 SSV9 的细胞受到保护而不会被杀死，并在种群中持续存在。我们假设，这种感染通过在具有多样化 CRISPR-Cas 免疫的种群中去除竞争者并确保病毒在种群内的垂直传播，成为宿主和病毒之间的一种共生形式。多项研究，尤其是那些专注于裂解病毒在关键模型系统中的作用的研究，已经表明了病毒在塑造微生物种群中的重要性。然而，越来越明显的是，与宿主长期相互作用的病毒，如慢性生活方式的病毒，可以成为进化的重要驱动因素，并对宿主生态学产生重大影响。在这项工作中，我们描述了与酸性古菌和其慢性病毒纺锤形病毒 9 之间的这种相互作用。我们的工作扩展了宿主和病毒共生进化的观点，描述了一种杀伤表型，我们假设这种表型的进化部分是由于在自然种群中观察到的 CRISPR-Cas 免疫的高流行率和多样性。我们探讨了这种表型在种群动态和宿主生态学中的意义，以及这种病毒-宿主对之间的共生关系的意义。
