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Elife. 2015 Jan 16;4:e05055. doi: 10.7554/eLife.05055.

The contrasting phylodynamics of human influenza B viruses.

Author information

1
Duke-NUS Graduate Medical School, Singapore, Singapore.
2
Marie Bashir Institute for Infectious Diseases and Biosecurity, University of Sydney, Sydney, Australia.
3
J Craig Venter Institute, Rockville, United States.
4
Bioinformatics Institute, Agency for Science, Technology and Research, Singapore, Singapore.
5
World Health Organisation Collaborating Centre for Reference and Research on Influenza, Peter Doherty Institute for Infection and Immunity, Melbourne, Australia.
6
Department of Environmental Systems Science, Eidgenössische Technische Hochschule Zürich, Zürich, Switzerland.
7
Department of Biosystems Science and Engineering, Eidgenössische Technische Hochschule Zürich, Zurich, Switzerland.
8
Royal Children's Hospital, Parkville, Australia.
9
Centre for Infectious Diseases and Microbiology Laboratory Services, Westmead Hospital and University of Sydney, Westmead, Australia.
10
Institute of Environmental Science and Research, National Centre for Biosecurity and Infectious Disease, Upper Hutt, New Zealand.
11
Microbiology Department, Canterbury Health Laboratories, Christchurch, New Zealand.
12
Virology Division, SEALS Microbiology, Prince of Wales Hospital, Sydney, Australia.

Abstract

A complex interplay of viral, host, and ecological factors shapes the spatio-temporal incidence and evolution of human influenza viruses. Although considerable attention has been paid to influenza A viruses, a lack of equivalent data means that an integrated evolutionary and epidemiological framework has until now not been available for influenza B viruses, despite their significant disease burden. Through the analysis of over 900 full genomes from an epidemiological collection of more than 26,000 strains from Australia and New Zealand, we reveal fundamental differences in the phylodynamics of the two co-circulating lineages of influenza B virus (Victoria and Yamagata), showing that their individual dynamics are determined by a complex relationship between virus transmission, age of infection, and receptor binding preference. In sum, this work identifies new factors that are important determinants of influenza B evolution and epidemiology.

KEYWORDS:

antigenic drift; epidemiology; evolution; evolutionary biology; genomics; human; infectious disease; influenza virus; microbiology; viruses

PMID:
25594904
PMCID:
PMC4383373
DOI:
10.7554/eLife.05055
[Indexed for MEDLINE]
Free PMC Article

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