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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

Influenza B virus lineages in Australia and New Zealand, 2001–2013and source of full genomes.Percentage prevalence of influenza B viruses isolated from the three easternAustralian states and New Zealand (A). Coloured lines representthe proportion of influenza viruses typed as influenza B in each country (blue)and each of the eastern Australian states; Queensland (yellow), New South Wales(orange), and Victoria (pink). Bars represent the percentage prevalence ofVictoria (black) and Yamagata (red). Data based on National Notifiable DiseasesSurveillance system (NNDSS) for Australia and Environmental Science andResearch (ESR) for New Zealand. The lineage of representative influenza B virusstrains used in the trivalent influenza vaccine during these years in bothcountries (B). Excluding the years 2003 and 2009, influenza Bviruses represented on average 24.6% (range 9.5–53.7%) and 31.5% (range0.5–86.9%) of laboratory confirmed influenza viruses from Australia andNew Zealand, respectively. The percentage of circulating influenza viruses thatwere influenza B was significantly lower in 2003 (AUS, 3.4%) and 2009 (AUS,0.8%) than in other years, due to the dominance of a new H3N2 variant(A/Fujian/412/2002-like) in 2003 and the emergence of the H1N1 pandemic in2009. Source of full genomes of Victoria and Yamagata viruses(C).DOI:http://dx.doi.org/10.7554/eLife.05055.004
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fig2: Influenza B virus lineages in Australia and New Zealand, 2001–2013and source of full genomes.Percentage prevalence of influenza B viruses isolated from the three easternAustralian states and New Zealand (A). Coloured lines representthe proportion of influenza viruses typed as influenza B in each country (blue)and each of the eastern Australian states; Queensland (yellow), New South Wales(orange), and Victoria (pink). Bars represent the percentage prevalence ofVictoria (black) and Yamagata (red). Data based on National Notifiable DiseasesSurveillance system (NNDSS) for Australia and Environmental Science andResearch (ESR) for New Zealand. The lineage of representative influenza B virusstrains used in the trivalent influenza vaccine during these years in bothcountries (B). Excluding the years 2003 and 2009, influenza Bviruses represented on average 24.6% (range 9.5–53.7%) and 31.5% (range0.5–86.9%) of laboratory confirmed influenza viruses from Australia andNew Zealand, respectively. The percentage of circulating influenza viruses thatwere influenza B was significantly lower in 2003 (AUS, 3.4%) and 2009 (AUS,0.8%) than in other years, due to the dominance of a new H3N2 variant(A/Fujian/412/2002-like) in 2003 and the emergence of the H1N1 pandemic in2009. Source of full genomes of Victoria and Yamagata viruses(C).DOI:http://dx.doi.org/10.7554/eLife.05055.004

Mentions: To understand the evolutionary and epidemiological dynamics of influenza B virus, wegenerated the full genomes of 908 influenza B viruses selected from over 26,000laboratory confirmed influenza B cases in children and adults aged from birth to 102years sampled during 2002–2013 in eastern Australia (Queensland,n = 275; New South Wales, n = 210;and Victoria, n = 207) and New Zealand (n= 216) (Figure 2). These regions wereselected because influenza surveillance was well established and continuous during thesampling period and included the co-circulation and periodic dominance of influenza Aand both influenza B virus lineages. Of note is that the influenza B virus strain usedfor vaccination in the region did not match the dominant circulating strain during 7 ofthe 13 years studied (Figure 2B). Our overall aimwas to integrate, for the first time, data obtained from genetic, epidemiological, andimmunological sources to better understand the evolution and interaction of these twolineages of influenza B virus.10.7554/eLife.05055.004Figure 2.Influenza B virus lineages in Australia and New Zealand, 2001–2013and source of full genomes.


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)

Influenza B virus lineages in Australia and New Zealand, 2001–2013and source of full genomes.Percentage prevalence of influenza B viruses isolated from the three easternAustralian states and New Zealand (A). Coloured lines representthe proportion of influenza viruses typed as influenza B in each country (blue)and each of the eastern Australian states; Queensland (yellow), New South Wales(orange), and Victoria (pink). Bars represent the percentage prevalence ofVictoria (black) and Yamagata (red). Data based on National Notifiable DiseasesSurveillance system (NNDSS) for Australia and Environmental Science andResearch (ESR) for New Zealand. The lineage of representative influenza B virusstrains used in the trivalent influenza vaccine during these years in bothcountries (B). Excluding the years 2003 and 2009, influenza Bviruses represented on average 24.6% (range 9.5–53.7%) and 31.5% (range0.5–86.9%) of laboratory confirmed influenza viruses from Australia andNew Zealand, respectively. The percentage of circulating influenza viruses thatwere influenza B was significantly lower in 2003 (AUS, 3.4%) and 2009 (AUS,0.8%) than in other years, due to the dominance of a new H3N2 variant(A/Fujian/412/2002-like) in 2003 and the emergence of the H1N1 pandemic in2009. Source of full genomes of Victoria and Yamagata viruses(C).DOI:http://dx.doi.org/10.7554/eLife.05055.004
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fig2: Influenza B virus lineages in Australia and New Zealand, 2001–2013and source of full genomes.Percentage prevalence of influenza B viruses isolated from the three easternAustralian states and New Zealand (A). Coloured lines representthe proportion of influenza viruses typed as influenza B in each country (blue)and each of the eastern Australian states; Queensland (yellow), New South Wales(orange), and Victoria (pink). Bars represent the percentage prevalence ofVictoria (black) and Yamagata (red). Data based on National Notifiable DiseasesSurveillance system (NNDSS) for Australia and Environmental Science andResearch (ESR) for New Zealand. The lineage of representative influenza B virusstrains used in the trivalent influenza vaccine during these years in bothcountries (B). Excluding the years 2003 and 2009, influenza Bviruses represented on average 24.6% (range 9.5–53.7%) and 31.5% (range0.5–86.9%) of laboratory confirmed influenza viruses from Australia andNew Zealand, respectively. The percentage of circulating influenza viruses thatwere influenza B was significantly lower in 2003 (AUS, 3.4%) and 2009 (AUS,0.8%) than in other years, due to the dominance of a new H3N2 variant(A/Fujian/412/2002-like) in 2003 and the emergence of the H1N1 pandemic in2009. Source of full genomes of Victoria and Yamagata viruses(C).DOI:http://dx.doi.org/10.7554/eLife.05055.004
Mentions: To understand the evolutionary and epidemiological dynamics of influenza B virus, wegenerated the full genomes of 908 influenza B viruses selected from over 26,000laboratory confirmed influenza B cases in children and adults aged from birth to 102years sampled during 2002–2013 in eastern Australia (Queensland,n = 275; New South Wales, n = 210;and Victoria, n = 207) and New Zealand (n= 216) (Figure 2). These regions wereselected because influenza surveillance was well established and continuous during thesampling period and included the co-circulation and periodic dominance of influenza Aand both influenza B virus lineages. Of note is that the influenza B virus strain usedfor vaccination in the region did not match the dominant circulating strain during 7 ofthe 13 years studied (Figure 2B). Our overall aimwas to integrate, for the first time, data obtained from genetic, epidemiological, andimmunological sources to better understand the evolution and interaction of these twolineages of influenza B virus.10.7554/eLife.05055.004Figure 2.Influenza B virus lineages in Australia and New Zealand, 2001–2013and source of full genomes.

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