tetano
Editor, Senior Moderator
J Infect Dis. 2018 Feb 9. doi: 10.1093/infdis/jiy082. [Epub ahead of print]
[h=1]Convergent Evolution of Human-Isolated H7N9 Avian Influenza A Viruses.[/h] Xiang D[SUP]1,[/SUP][SUP]2[/SUP], Shen X[SUP]1[/SUP], Pu Z[SUP]1[/SUP], Irwin DM[SUP]3,[/SUP][SUP]4[/SUP], Liao M[SUP]1,[/SUP][SUP]5[/SUP], Shen Y[SUP]1,[/SUP][SUP]2,[/SUP][SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]Background:[/h] Avian influenza A virus (AIV) H7N9 has caused five epidemic waves of human infections in China since 2013. AIVs may face strong selection to adapt to novel conditions when establishing themselves in humans. In this study, we sought to determine whether adaptive evolution had occurred in human-isolated H7N9 viruses.
[h=4]Methods:[/h] We evaluated all available genomes of H7N9 AIVs. Maximum likelihood trees were separately reconstructed for all eight genes. Signals of positive selection and convergent evolution were then detected on branches that lead to changes in host tropism (from avian to human).
[h=4]Results:[/h] We found that three genes had significant signals of positive selection. In addition, we detected 34 sites having significant signals for parallel evolution in eight genes, including seven well-known sites (Q591K, E627K and D701N in PB2 gene, R156K, V202A and L244Q in HA, and R289K in NA) that play roles in crossing species barriers for AIVs.
[h=4]Conclusion:[/h] Our study suggests that during infection in humans, H7N9 viruses have undergone adaptive evolution to adapt to their new host environment, and that the sites where parallel evolution occurred might play roles in crossing species barriers and respond to the new selection pressures arising from their new host environments.
[h=4]KEYWORDS:[/h] H7N9; convergent evolution; host shift; human infection
PMID: 29438519 DOI: 10.1093/infdis/jiy082
[h=1]Convergent Evolution of Human-Isolated H7N9 Avian Influenza A Viruses.[/h] Xiang D[SUP]1,[/SUP][SUP]2[/SUP], Shen X[SUP]1[/SUP], Pu Z[SUP]1[/SUP], Irwin DM[SUP]3,[/SUP][SUP]4[/SUP], Liao M[SUP]1,[/SUP][SUP]5[/SUP], Shen Y[SUP]1,[/SUP][SUP]2,[/SUP][SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]Background:[/h] Avian influenza A virus (AIV) H7N9 has caused five epidemic waves of human infections in China since 2013. AIVs may face strong selection to adapt to novel conditions when establishing themselves in humans. In this study, we sought to determine whether adaptive evolution had occurred in human-isolated H7N9 viruses.
[h=4]Methods:[/h] We evaluated all available genomes of H7N9 AIVs. Maximum likelihood trees were separately reconstructed for all eight genes. Signals of positive selection and convergent evolution were then detected on branches that lead to changes in host tropism (from avian to human).
[h=4]Results:[/h] We found that three genes had significant signals of positive selection. In addition, we detected 34 sites having significant signals for parallel evolution in eight genes, including seven well-known sites (Q591K, E627K and D701N in PB2 gene, R156K, V202A and L244Q in HA, and R289K in NA) that play roles in crossing species barriers for AIVs.
[h=4]Conclusion:[/h] Our study suggests that during infection in humans, H7N9 viruses have undergone adaptive evolution to adapt to their new host environment, and that the sites where parallel evolution occurred might play roles in crossing species barriers and respond to the new selection pressures arising from their new host environments.
[h=4]KEYWORDS:[/h] H7N9; convergent evolution; host shift; human infection
PMID: 29438519 DOI: 10.1093/infdis/jiy082