Adaptive evolution and environmental durability jointly structure phylodynamic patterns in avian influenza viruses.

Benjamin Roche,David E Stallknecht,Justin Brown,John M Drake,Pejman Rohani,Trevor Bedford,Christophe Fraser

doi:10.1371/journal.pbio.1001931

Abstract

Author SummaryHuman populations have experienced several pandemics involving new subtypes of influenza virus over the past century. All of these pandemic strains contained gene segments that originated in wild birds, a host pool that supports a very large and genetically diverse array of influenza viruses. However, once an avian strain establishes itself within the human population, the genetic diversity of the resulting human subtypes is typically quite low compared to that of their avian counterparts. Here we compare the evolutionary dynamics of human and avian influenza viruses in North America and test different hypotheses that might explain these two contrasting evolutionary patterns. Our analysis shows that a combination of characteristics of the host (especially demography) and virus (such as durability in water and mutability) explains the diversity observed. Using a theoretical model, we show that the combination of the short lifespan of wild birds, and greater durability of viruses in aquatic environments, is key to maintaining the high levels of influenza diversity observed in wild birds.

Highlights

Seasonal epidemics of influenza viruses are responsible for significant human morbidity and mortality [1]
We show that the combination of the short lifespan of wild birds, and greater durability of viruses in aquatic environments, is key to maintaining the high levels of influenza diversity observed in wild birds
avian influenza viruses (AIVs) typically exhibit a scaled effective population size (Net, which measures the phylogenetic diversity of the virus population [16]) that is an order of magnitude greater than for their human counterparts: We estimated Net to be 7.0 y and 1.5 y, respectively, for H1 and H3 in humans and 38.7 y and 77.5 y in birds (Figure 1E and 1F; as we show below, other avian subtypes exhibit higher diversity than commonly observed in H1 and H3 human subtypes)

Summary

Introduction

Seasonal epidemics of influenza viruses are responsible for significant human morbidity and mortality [1]. Human influenza viruses exhibit very limited subtype diversity (Figure 1C), as defined by the number of serologically distinct hemagglutinin (H or HA) glycoprotein types [9], where only H1 and H3 subtypes of influenza A viruses have significantly circulated since 1968 [15]. In addition to this paucity of subtypes, genetic diversity is limited within H1 (Figure 1E) and H3 (Figure 1F) subtypes, as reflected in the slender trunk of the consensus phylogenetic tree (Figure 1I and 1J)

Methods

Results

Conclusion