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The contrasting phylodynamics of human influenza B viruses.

Vijaykrishna D, Holmes EC, Joseph U, Fourment M, Su YC, Halpin R, Lee RT, Deng YM, Gunalan V, Lin X, Stockwell TB, Fedorova NB, Zhou B, Spirason N, Kühnert D, Bošková V, Stadler T, Costa AM, Dwyer DE, Huang QS, Jennings LC, Rawlinson W, Sullivan SG, Hurt AC, Maurer-Stroh S, Wentworth DE, Smith GJ, Barr IG - Elife (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Duke-NUS Graduate Medical School, Singapore, Singapore.

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.

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Related in: MedlinePlus

Effect of sampling on the population dynamics of Influenza Bvirus.Relative genetic diversity of the Victoria (black) and Yamagata (red)lineages estimated using the Gaussian Markov Random Fields (GMRF) Skyridemodel (as in Figure 3), using asubsampled Victoria data set, in which, the number of Victoria lineageviruses was randomly reduced to match the size of Yamagata for thatyear.DOI:http://dx.doi.org/10.7554/eLife.05055.006
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fig3s1: Effect of sampling on the population dynamics of Influenza Bvirus.Relative genetic diversity of the Victoria (black) and Yamagata (red)lineages estimated using the Gaussian Markov Random Fields (GMRF) Skyridemodel (as in Figure 3), using asubsampled Victoria data set, in which, the number of Victoria lineageviruses was randomly reduced to match the size of Yamagata for thatyear.DOI:http://dx.doi.org/10.7554/eLife.05055.006

Mentions: We used the HA segment of both lineages to contrast their phylodynamics. First, toassess the changing patterns of genetic diversity of the two influenza B viruslineages in relation to their evolutionary histories, we used a flexiblecoalescent-based demographic model (Minin et al.,2008), which revealed stark differences in the epidemiological dynamics ofthe Victoria and Yamagata lineages (Figure3A,B). Whereas the Victoria lineage experienced strong seasonalfluctuations in relative genetic diversity, little change was observed over the sametime period for the Yamagata lineage, and these observations were not heavilyaffected by differences in sampling density (Figure3—figure supplement 1). While the almost invariant relative geneticdiversity of the Yamagata lineage resembled that of seasonal H1N1 viruses (Figure 3D), the stark and almost annual changesof diversity in the Victoria lineage were similar to those observed for H3N2 virus(Figure 3C); although H3N2 virusesexhibited a greater frequency of oscillations than those estimated for Victorialineage viruses. The strong seasonal fluctuations in diversity observed for Victorialineage suggest that this lineage experiences strong bottlenecks between seasonssimilar to those described for H3N2 viruses (Bedfordet al., 2011; Zinder et al.,2013), whereas the almost invariant relative genetic diversity for Yamagatasuggests the continuous co-circulation of multiple lineages.10.7554/eLife.05055.005Figure 3.Population dynamics of genetic diversity in Australia and NewZealand.


The contrasting phylodynamics of human influenza B viruses.

Vijaykrishna D, Holmes EC, Joseph U, Fourment M, Su YC, Halpin R, Lee RT, Deng YM, Gunalan V, Lin X, Stockwell TB, Fedorova NB, Zhou B, Spirason N, Kühnert D, Bošková V, Stadler T, Costa AM, Dwyer DE, Huang QS, Jennings LC, Rawlinson W, Sullivan SG, Hurt AC, Maurer-Stroh S, Wentworth DE, Smith GJ, Barr IG - Elife (2015)

Effect of sampling on the population dynamics of Influenza Bvirus.Relative genetic diversity of the Victoria (black) and Yamagata (red)lineages estimated using the Gaussian Markov Random Fields (GMRF) Skyridemodel (as in Figure 3), using asubsampled Victoria data set, in which, the number of Victoria lineageviruses was randomly reduced to match the size of Yamagata for thatyear.DOI:http://dx.doi.org/10.7554/eLife.05055.006
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4383373&req=5

fig3s1: Effect of sampling on the population dynamics of Influenza Bvirus.Relative genetic diversity of the Victoria (black) and Yamagata (red)lineages estimated using the Gaussian Markov Random Fields (GMRF) Skyridemodel (as in Figure 3), using asubsampled Victoria data set, in which, the number of Victoria lineageviruses was randomly reduced to match the size of Yamagata for thatyear.DOI:http://dx.doi.org/10.7554/eLife.05055.006
Mentions: We used the HA segment of both lineages to contrast their phylodynamics. First, toassess the changing patterns of genetic diversity of the two influenza B viruslineages in relation to their evolutionary histories, we used a flexiblecoalescent-based demographic model (Minin et al.,2008), which revealed stark differences in the epidemiological dynamics ofthe Victoria and Yamagata lineages (Figure3A,B). Whereas the Victoria lineage experienced strong seasonalfluctuations in relative genetic diversity, little change was observed over the sametime period for the Yamagata lineage, and these observations were not heavilyaffected by differences in sampling density (Figure3—figure supplement 1). While the almost invariant relative geneticdiversity of the Yamagata lineage resembled that of seasonal H1N1 viruses (Figure 3D), the stark and almost annual changesof diversity in the Victoria lineage were similar to those observed for H3N2 virus(Figure 3C); although H3N2 virusesexhibited a greater frequency of oscillations than those estimated for Victorialineage viruses. The strong seasonal fluctuations in diversity observed for Victorialineage suggest that this lineage experiences strong bottlenecks between seasonssimilar to those described for H3N2 viruses (Bedfordet al., 2011; Zinder et al.,2013), whereas the almost invariant relative genetic diversity for Yamagatasuggests the continuous co-circulation of multiple lineages.10.7554/eLife.05055.005Figure 3.Population dynamics of genetic diversity in Australia and NewZealand.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Duke-NUS Graduate Medical School, Singapore, Singapore.

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.

Show MeSH
Related in: MedlinePlus