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.
Highlights
In addition to two subtypes of influenza A virus (H1N1 and H3N2), two lineages of influenza B viruses co-circulate in humans and cause seasonal influenza epidemics (Klimov et al, 2012)
While the almost invariant relative genetic diversity of the Yamagata lineage resembled that of seasonal H1N1 viruses (Figure 3D), the stark and almost annual changes of diversity in the Victoria lineage were similar to those observed for H3N2 virus (Figure 3C); H3N2 viruses exhibited a greater frequency of oscillations than those estimated for Victoria lineage viruses
The strong seasonal fluctuations in diversity observed for Victoria lineage suggest that this lineage experiences strong bottlenecks between seasons similar to those described for H3N2 viruses (Bedford et al, 2011; Zinder et al, 2013), whereas the almost invariant relative genetic diversity for Yamagata suggests the continuous co-circulation of multiple lineages
Summary
In addition to two subtypes of influenza A virus (H1N1 and H3N2), two lineages of influenza B viruses co-circulate in humans and cause seasonal influenza epidemics (Klimov et al, 2012). Type A and B influenza viruses are closely related and have similarities in genome organization and protein structure (McCauley et al, 2012), they exhibit important differences in their ecology and evolution (Chen and Holmes, 2008; Tan et al, 2013). While new influenza A viruses periodically emerge from animal reservoirs to become endemic in humans (Neumann et al, 2009; Smith et al, 2009), influenza B viruses, first recognized in 1940, have circulated continuously in humans alongside influenza A viruses and are presumably derived from a single, as yet unknown, source (Francis, 1940; Chen and Holmes, 2008). While the evolutionary and epidemiological dynamics of human influenza A H1N1 and H3N2 viruses have been well documented at the global scale (Rambaut et al, 2008; Russell et al, 2008; Bedford et al, 2010; Bahl et al, 2011), the equivalent dynamics of the two influenza B virus lineages—B/Yamagata/16/88-like and B/Victoria/2/87-like, termed the Yamagata and Victoria viruses—are poorly understood
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