dorsal/arxiv
View SchemaPhenotypic mixing and hiding may contribute to memory in viral quasispecies
| Authors | Claus O. Wilke, Isabel S. Novella |
|---|---|
| Categories | |
| ArXiv ID | physics/0306184 |
| URL | https://arxiv.org/abs/physics/0306184 |
| Journal | BMC Microbiology 3:11 (2003) |
Abstract
Background. In a number of recent experiments with food-and-mouth disease virus, a deleterious mutant, was found to avoid extinction and remain in the population for long periods of time. This observation was called quasispecies memory. The origin of quasispecies memory is not fully understood. Results. We propose and analyze a simple model of complementation between the wild type virus and a mutant that has an impaired ability of cell entry. The mutant will go extinct unless it is recreated from the wild type through mutations. However, under phenotypic mixing-and-hiding as a mechanism of complementation, the time to extinction in the absence of mutations increases with increasing multiplicity of infection (m.o.i.). The mutant's frequency at equilibrium under selection-mutation balance also increases with increasing m.o.i. At high m.o.i., a large fraction of mutant genomes are encapsidated with wild-type protein, which enables them to infect cells as efficiently as the wild type virions, and thus increases their fitness to the wild-type level. Moreover, even at low m.o.i. the equilibrium frequency of the mutant is higher than predicted by the standard quasispecies model, because a fraction of mutant virions generated from wild-type parents will also be encapsidated by wild-type protein. Conclusions. Our model predicts that phenotypic hiding will strongly influence the population dynamics of viruses, particularly at high m.o.i., and will also have important effects on the mutation--selection balance at low m.o.i. The delay in mutant extinction and increase in mutant frequencies at equilibrium may, at least in part, explain memory in quasispecies populations.
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"abstract": "Background. In a number of recent experiments with food-and-mouth disease\nvirus, a deleterious mutant, was found to avoid extinction and remain in the\npopulation for long periods of time. This observation was called quasispecies\nmemory. The origin of quasispecies memory is not fully understood.\n Results. We propose and analyze a simple model of complementation between the\nwild type virus and a mutant that has an impaired ability of cell entry. The\nmutant will go extinct unless it is recreated from the wild type through\nmutations. However, under phenotypic mixing-and-hiding as a mechanism of\ncomplementation, the time to extinction in the absence of mutations increases\nwith increasing multiplicity of infection (m.o.i.). The mutant\u0027s frequency at\nequilibrium under selection-mutation balance also increases with increasing\nm.o.i. At high m.o.i., a large fraction of mutant genomes are encapsidated with\nwild-type protein, which enables them to infect cells as efficiently as the\nwild type virions, and thus increases their fitness to the wild-type level.\nMoreover, even at low m.o.i. the equilibrium frequency of the mutant is higher\nthan predicted by the standard quasispecies model, because a fraction of mutant\nvirions generated from wild-type parents will also be encapsidated by wild-type\nprotein.\n Conclusions. Our model predicts that phenotypic hiding will strongly\ninfluence the population dynamics of viruses, particularly at high m.o.i., and\nwill also have important effects on the mutation--selection balance at low\nm.o.i. The delay in mutant extinction and increase in mutant frequencies at\nequilibrium may, at least in part, explain memory in quasispecies populations.",
"arxiv_id": "physics/0306184",
"authors": [
"Claus O. Wilke",
"Isabel S. Novella"
],
"categories": [
"physics.bio-ph",
"cond-mat.soft",
"nlin.AO",
"q-bio.PE"
],
"journal_ref": "BMC Microbiology 3:11 (2003)",
"title": "Phenotypic mixing and hiding may contribute to memory in viral quasispecies",
"url": "https://arxiv.org/abs/physics/0306184"
},
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