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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

Year-wise age distribution of influenza B viruses.Mean and median of age distribution of influenza B viruses(A). Box-whisker plot with mean (square) and agedistribution of all influenza B viruses cases (jitter plot) are shown foryears with greater than 100 samples for either lineage(B).DOI:http://dx.doi.org/10.7554/eLife.05055.016
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fig10s1: Year-wise age distribution of influenza B viruses.Mean and median of age distribution of influenza B viruses(A). Box-whisker plot with mean (square) and agedistribution of all influenza B viruses cases (jitter plot) are shown foryears with greater than 100 samples for either lineage(B).DOI:http://dx.doi.org/10.7554/eLife.05055.016

Mentions: In addition to genetic, antigenic, and evolutionary differences, we found a notabledifference in the age distribution of infected cases for the two influenza B viruslineages (Figure 10) that was generallyconsistent throughout our sampling period (Figure10—figure supplement 1). On average, Victoria viruses infected ayounger population (mean 16.8 years, median 11 years) compared to Yamagata viruses(mean 26.6 years, median 18 years). Although the proportion of cases under 6 yearswere similar in both lineages (28.8% of Victoria and 26.8% of Yamagata), there were1.7 times more cases aged 6–17 years infected with a Victoria lineage virus(39.0% Victoria vs 22.7% Yamagata), while this ratio was almost reversed for thoseaged 18 years and over (32.2% Victoria vs 50.0% Yamagata;χ2, p < 0.0001) (Table 2). Thus, nearly 70% of Victoria lineage viruses wereidentified in children <18 years, whereas the Yamagata lineage exhibited abimodal age distribution with a significant shift toward infections in individualsaged >25 years (Figure 10). Thesedifferences in age distribution are significant and unlikely to be explained bysystematic bias because the same pattern was observed in both countries, and areconsistent with data from Guangdong, China (Tan etal., 2013), and Slovenia (Sočan etal., 2014) during the 2009–2010 and 2010–2013 epidemicseasons, respectively.10.7554/eLife.05055.015Figure 10.Age distribution 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)

Year-wise age distribution of influenza B viruses.Mean and median of age distribution of influenza B viruses(A). Box-whisker plot with mean (square) and agedistribution of all influenza B viruses cases (jitter plot) are shown foryears with greater than 100 samples for either lineage(B).DOI:http://dx.doi.org/10.7554/eLife.05055.016
© Copyright Policy
Related In: Results  -  Collection

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

fig10s1: Year-wise age distribution of influenza B viruses.Mean and median of age distribution of influenza B viruses(A). Box-whisker plot with mean (square) and agedistribution of all influenza B viruses cases (jitter plot) are shown foryears with greater than 100 samples for either lineage(B).DOI:http://dx.doi.org/10.7554/eLife.05055.016
Mentions: In addition to genetic, antigenic, and evolutionary differences, we found a notabledifference in the age distribution of infected cases for the two influenza B viruslineages (Figure 10) that was generallyconsistent throughout our sampling period (Figure10—figure supplement 1). On average, Victoria viruses infected ayounger population (mean 16.8 years, median 11 years) compared to Yamagata viruses(mean 26.6 years, median 18 years). Although the proportion of cases under 6 yearswere similar in both lineages (28.8% of Victoria and 26.8% of Yamagata), there were1.7 times more cases aged 6–17 years infected with a Victoria lineage virus(39.0% Victoria vs 22.7% Yamagata), while this ratio was almost reversed for thoseaged 18 years and over (32.2% Victoria vs 50.0% Yamagata;χ2, p < 0.0001) (Table 2). Thus, nearly 70% of Victoria lineage viruses wereidentified in children <18 years, whereas the Yamagata lineage exhibited abimodal age distribution with a significant shift toward infections in individualsaged >25 years (Figure 10). Thesedifferences in age distribution are significant and unlikely to be explained bysystematic bias because the same pattern was observed in both countries, and areconsistent with data from Guangdong, China (Tan etal., 2013), and Slovenia (Sočan etal., 2014) during the 2009–2010 and 2010–2013 epidemicseasons, respectively.10.7554/eLife.05055.015Figure 10.Age distribution 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