Heterogeneity in antibody range and the antigenic drift of influenza A viruses |
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| Affiliation: | 1. Centro de Física da Matéria Condensada and Departamento de Física, Faculdade de Ciências da Universidade de Lisboa, P-1649-003 Lisboa Codex, Portugal;2. Instituto Gulbenkian de Ciência, P-2781-901 Oeiras, Portugal;1. Health Protection Team, Public Health England North West, Manchester, UK;2. Health Protection Team, Public Health England Yorkshire and the Humber, Leeds, UK;3. Virus Reference Unit, National Infection Service, Public Health England, London, UK;4. Manchester Academic Health Science Centre, University of Manchester, UK;5. Centre of Infectious Disease Surveillance and Control, National Infection Service, Public Health England, London, UK;1. Institute of Medical Virology, Wuhan University School of Basic Medical Sciences, Wuhan, 430072, China;2. Division for Viral Disease Detection, Hubei Provincial Center for Disease Control and Prevention, Wuhan, 430079, China;3. College of Medicine, Wuhan university of Science and Technology, Wuhan, 430081, China;1. Instituto de Física, Universidade Federal da Bahia, Campus Universitário de Ondina, 40210-340, Salvador, Brazil;2. Departamento de Matemática and Centro de Matemática e Aplicações, Universidade Nova de Lisboa, Quinta da Torre, 2829-516, Caparica, Portugal;3. Faculdade de Educação, Universidade Federal da Grande Dourados, Rodovia Dourados, Itahum, km 12, 79804-070 - Dourados, Brazil;4. Instituto Gulbenkian de Ciência, Oeiras, Portugal |
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| Abstract: | In this paper we explore the consequences of a heterogeneous immune response in individuals on the evolution of a rapidly mutating virus. We show that several features of the incidence and phylogenetic patterns typical of influenza A may be understood in this framework. In our model, limited diversity and rapid drift of the circulating viral strains result from the interplay of two interacting subpopulations with different types of immune response, narrow or broad, upon infection. The subpopulation with the narrow immune response acts as a reservoir where consecutive mutations escape immunity and can persist. Strains with a number of accumulated mutations escape immunity in the other subpopulation as well, causing larger epidemic peaks in the whole population, and reducing strain diversity. Overall, our model produces a modulation of epidemic peak heights and patterns of antigenic drift consistent with reported observations, suggesting an underlying mechanism for the evolutionary epidemiology of influenza, in particular, and other infectious diseases, more generally. |
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