Reassortment patterns of avian influenza virus internal segments among different subtypes.
BACKGROUND
The segmented RNA genome of avian Influenza viruses (AIV) allows genetic reassortment between co-infecting viruses, providing an evolutionary pathway to generate genetic innovation. The genetic diversity (16 haemagglutinin and 9 neuraminidase subtypes) of AIV indicates an extensive reservoir of influenza viruses exists in bird populations, but how frequently subtypes reassort with each other is still unknown. Here we quantify the reassortment patterns among subtypes in the Eurasian avian viral pool by reconstructing the ancestral states of the subtypes as discrete states on time-scaled phylogenies with respect to the internal protein coding segments. We further analyzed how host species, the inferred evolutionary rates and the dN/dS ratio varied among segments and between discrete subtypes, and whether these factors may be associated with inter-subtype reassortment rate.


RESULTS
The general patterns of reassortment are similar among five internal segments with the exception of segment 8, encoding the Non-Structural genes, which has a more divergent phylogeny. However, significant variation in rates between subtypes was observed. In particular, hemagglutinin-encoding segments of subtypes H5 to H9 reassort at a lower rate compared to those of H1 to H4, and Neuraminidase-encoding segments of subtypes N1 and N2 reassort less frequently than N3 to N9. Both host species and dN/dS ratio were significantly associated with reassortment rate, while evolutionary rate was not associated. The dN/dS ratio was negatively correlated with reassortment rate, as was the number of negatively selected sites for all segments.


CONCLUSIONS
These results indicate that overall selective constraint and host species are both associated with reassortment rate. These results together identify the wild bird population as the major source of new reassortants, rather than domestic poultry. The lower reassortment rates observed for H5N1 and H9N2 may be explained by the large proportion of strains derived from domestic poultry populations. In contrast, the higher rates observed in the H1N1, H3N8 and H4N6 subtypes could be due to their primary origin as infections of wild birds with multiple low pathogenicity strains in the large avian reservoir.
Lu
L
Lu
Samantha J
SJ
Lycett
University of Edinburgh, Institute of Evolutionary Biology, Ashworth Laboratories, West Mains Road, Edinburgh EH9 3JT, UK. A.Leigh-Brown@ed.ac.uk.
Andrew J
AJ
Leigh Brown
D000818:Animals; D001717:Birds; D019143:Evolution, Molecular; D014644:Genetic Variation; D019267:Hemagglutinin Glycoproteins, Influenza Virus / Q000235:genetics*; D058507:Host Specificity; D009980:Influenza A virus / Q000145:classification / Q000201:enzymology / Q000235:genetics* / Q000502:physiology; D005585:Influenza in Birds / Q000821:virology*; D008969:Molecular Sequence Data; D009439:Neuraminidase / Q000235:genetics*; D010802:Phylogeny; D011995:Recombination, Genetic; D014764:Viral Proteins / Q000235:genetics*
D019267:Hemagglutinin Glycoproteins, Influenza Virus; D014764:Viral Proteins; C109963:hemagglutinin, avian influenza A virus; C487630:NA protein, influenza A virus; D009439:Neuraminidase