Limits...
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.

Show MeSH

Related in: MedlinePlus

Evolution of the hemagglutinin genes of influenza B viruses.Phylogenetic relationship of the HA genes of influenza B Victoria (black)and Yamagata (red) lineage viruses inferred using the uncorrelated lognormalrelaxed clock model. Genetic diversity through time was estimated byaveraging the pairwise distance in time between random contemporaneoussamples with a 1-month window on the same dated Maximum clade credibility(MCC) trees.DOI:http://dx.doi.org/10.7554/eLife.05055.007
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4383373&req=5

fig4: Evolution of the hemagglutinin genes of influenza B viruses.Phylogenetic relationship of the HA genes of influenza B Victoria (black)and Yamagata (red) lineage viruses inferred using the uncorrelated lognormalrelaxed clock model. Genetic diversity through time was estimated byaveraging the pairwise distance in time between random contemporaneoussamples with a 1-month window on the same dated Maximum clade credibility(MCC) trees.DOI:http://dx.doi.org/10.7554/eLife.05055.007

Mentions: Marked differences between the Victoria and Yamagata lineages were apparent inphylogenetic trees of the HA (Figure 4). Thephylogenetic analysis of the HA genes showed that the Victoria lineage wascharacterized by a single prominent tree ‘trunk’, with side branchesthat circulated for short periods of time (1–3 years) (Figure 4). This evolutionary pattern parallels that observed forseasonal H3N2 viruses and is indicative of frequent selective bottlenecks due to theserial replacement of circulating strains, as would be expected under continualantigenic drift (Grenfell et al., 2004). Incontrast, greater diversification was observed for the Yamagata lineage, withmultiple clades co-circulating for extensive periods of time (Figure 4). For example, the three clades of Yamagata virusescirculating in 2013 diverged approximately 10 years ago, again paralleling theevolutionary pattern seen in seasonal H1N1 viruses. These patterns are clearlyidentifiable in the genealogical diversity skyline (Figure 4) in which the average time to common ancestor betweencontemporaneous samples fluctuated from 0 to <5 years for Victoria lineage,except during 2010 and 2011 where the genealogical diversity marginally increased to7 years. In contrast, the genealogical diversity of Yamagata was consistently greaterand gradually increased during the sampling period. The maintenance of geneticdiversity through epidemic peaks and troughs as described for Yamagata (Figure 3B) is expected to result in the gradualincrease of divergence times of contemporaneous samples.10.7554/eLife.05055.007Figure 4.Evolution of the hemagglutinin genes of influenza B viruses.


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)

Evolution of the hemagglutinin genes of influenza B viruses.Phylogenetic relationship of the HA genes of influenza B Victoria (black)and Yamagata (red) lineage viruses inferred using the uncorrelated lognormalrelaxed clock model. Genetic diversity through time was estimated byaveraging the pairwise distance in time between random contemporaneoussamples with a 1-month window on the same dated Maximum clade credibility(MCC) trees.DOI:http://dx.doi.org/10.7554/eLife.05055.007
© Copyright Policy
Related In: Results  -  Collection

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

fig4: Evolution of the hemagglutinin genes of influenza B viruses.Phylogenetic relationship of the HA genes of influenza B Victoria (black)and Yamagata (red) lineage viruses inferred using the uncorrelated lognormalrelaxed clock model. Genetic diversity through time was estimated byaveraging the pairwise distance in time between random contemporaneoussamples with a 1-month window on the same dated Maximum clade credibility(MCC) trees.DOI:http://dx.doi.org/10.7554/eLife.05055.007
Mentions: Marked differences between the Victoria and Yamagata lineages were apparent inphylogenetic trees of the HA (Figure 4). Thephylogenetic analysis of the HA genes showed that the Victoria lineage wascharacterized by a single prominent tree ‘trunk’, with side branchesthat circulated for short periods of time (1–3 years) (Figure 4). This evolutionary pattern parallels that observed forseasonal H3N2 viruses and is indicative of frequent selective bottlenecks due to theserial replacement of circulating strains, as would be expected under continualantigenic drift (Grenfell et al., 2004). Incontrast, greater diversification was observed for the Yamagata lineage, withmultiple clades co-circulating for extensive periods of time (Figure 4). For example, the three clades of Yamagata virusescirculating in 2013 diverged approximately 10 years ago, again paralleling theevolutionary pattern seen in seasonal H1N1 viruses. These patterns are clearlyidentifiable in the genealogical diversity skyline (Figure 4) in which the average time to common ancestor betweencontemporaneous samples fluctuated from 0 to <5 years for Victoria lineage,except during 2010 and 2011 where the genealogical diversity marginally increased to7 years. In contrast, the genealogical diversity of Yamagata was consistently greaterand gradually increased during the sampling period. The maintenance of geneticdiversity through epidemic peaks and troughs as described for Yamagata (Figure 3B) is expected to result in the gradualincrease of divergence times of contemporaneous samples.10.7554/eLife.05055.007Figure 4.Evolution of the hemagglutinin genes of influenza B viruses.

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