The Roles of Competition and Mutation in Shaping Antigenic and Genetic Diversity in Influenza
Identifieur interne : 000820 ( Main/Exploration ); précédent : 000819; suivant : 000821The Roles of Competition and Mutation in Shaping Antigenic and Genetic Diversity in Influenza
Auteurs : Daniel Zinder [États-Unis] ; Trevor Bedford [Royaume-Uni] ; Sunetra Gupta [Royaume-Uni] ; Mercedes Pascual [États-Unis]Source :
- PLoS Pathogens [ 1553-7366 ] ; 2013.
Abstract
Influenza A (H3N2) offers a well-studied, yet not fully understood, disease in terms of the interactions between pathogen population dynamics, epidemiology and genetics. A major open question is why the virus population is globally dominated by a single and very recently diverged (2–8 years) lineage. Classically, this has been modeled by limiting the generation of new successful antigenic variants, such that only a small subset of progeny acquire the necessary mutations to evade host immunity. An alternative approach was recently suggested by Recker et al. in which a limited number of antigenic variants are continuously generated, but most of these are suppressed by pre-existing host population immunity. Here we develop a framework spanning the regimes described above to explore the impact of rates of mutation and levels of competition on phylodynamic patterns. We find that the evolutionary dynamics of the subtype H3N2 influenza is most easily generated within this framework when it is mutation limited as well as being under strong immune selection at a number of epitope regions of limited diversity.
Url:
DOI: 10.1371/journal.ppat.1003104
PubMed: 23300455
PubMed Central: 3536651
Affiliations:
- Royaume-Uni, États-Unis
- Angleterre, Michigan, Nouveau-Mexique, Oxfordshire, Écosse
- Oxford, Édimbourg
- Université d'Oxford, Université d'Édimbourg
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<front><div type="abstract" xml:lang="en"><p>Influenza A (H3N2) offers a well-studied, yet not fully understood, disease in terms of the interactions between pathogen population dynamics, epidemiology and genetics. A major open question is why the virus population is globally dominated by a single and very recently diverged (2–8 years) lineage. Classically, this has been modeled by limiting the generation of new successful antigenic variants, such that only a small subset of progeny acquire the necessary mutations to evade host immunity. An alternative approach was recently suggested by Recker et al. in which a limited number of antigenic variants are continuously generated, but most of these are suppressed by pre-existing host population immunity. Here we develop a framework spanning the regimes described above to explore the impact of rates of mutation and levels of competition on phylodynamic patterns. We find that the evolutionary dynamics of the subtype H3N2 influenza is most easily generated within this framework when it is mutation limited as well as being under strong immune selection at a number of epitope regions of limited diversity.</p>
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