| Literature DB >> 27683365 |
Hayriye Gulbudak1, Joshua S Weitz2.
Abstract
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.Entities:
Keywords: dormancy; microbes; nonlinear dynamics; viruses
Year: 2016 PMID: 27683365 PMCID: PMC5046894 DOI: 10.1098/rspb.2016.1037
Source DB: PubMed Journal: Proc Biol Sci ISSN: 0962-8452 Impact factor: 5.349