A touch of sleep: biophysical model of contact-mediated dormancy of archaea by viruses

A touch of sleep: biophysical model of contact-mediated dormancy of archaea by viruses
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一丝睡眠:病毒接触介导的古细菌休眠的生物物理模型

DOI:
10.1098/rspb.2016.1037
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发表时间:
2015
期刊:
Proceedings of the Royal Society B: Biological Sciences
影响因子:
--
通讯作者:
J. Weitz
J. Weitz
中科院分区:
--
文献类型:
--
作者:
H. Gulbudak;J. Weitz

文献摘要

被引文献

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关于病毒与其微生物宿主之间相互作用的经典观点认为,宿主和病毒命运的变化需要病毒开始感染宿主。感染可导致宿主细胞死亡和病毒释放,通过细胞防御机制消除病毒基因组或病毒基因组作为染色体或染色体外元件与宿主整合。在这里,我们重新审视这一经典观点,灵感来自最近的实验发现,其中大多数靶宿主细胞可以被诱导进入休眠状态时,暴露于活性或灭活病毒,即使当病毒存在于低相对滴度。我们建议,无论是定性的现象和定量的休眠诱导的时间尺度是一致的假设,即细胞生理学可以通过接触宿主细胞的表面上,而不是严格的感染改变。为了验证这一假设,我们开发和研究了一个生物物理模型的接触介导的动态涉及病毒颗粒和靶细胞。我们展示了病毒颗粒如何催化许多细胞之间的细胞转化,即使它们最终只感染一个(或不感染)。我们还发现,人口规模的休眠是强大的模型动态,包括细胞生长,死亡和恢复的代表性的变化。
The canonical view of the interactions between viruses and their microbial hosts presumes that changes in host and virus fate requires the initiation of infection of a host by a virus. Infection may lead to the death of the host cell and release of viruses, to the elimination of the viral genome through cellular defence mechanisms or the integration of the viral genome with the host as a chromosomal or extrachromosomal element. Here, we revisit this canonical view, inspired by recent experimental findings in which the majority of target host cells can be induced into a dormant state when exposed to either active or deactivated viruses, even when viruses are present at low relative titre. We propose that both the qualitative phenomena and the quantitative timescales of dormancy induction are consistent with the hypothesis that cellular physiology can be altered by contact on the surface of host cells rather than strictly by infection. In order to test this hypothesis, we develop and study a biophysical model of contact-mediated dynamics involving virus particles and target cells. We show how virus particles can catalyse cellular transformations among many cells, even if they ultimately infect only one (or none). We also find that population-scale dormancy is robust to variation in the representation of model dynamics, including cell growth, death and recovery.