tetano
Editor, Senior Moderator
J Virol. 2019 May 8. pii: JVI.00543-19. doi: 10.1128/JVI.00543-19. [Epub ahead of print]
[h=1]Loss of fitness in mallards of Mexican H7N3 highly pathogenic avian influenza virus after circulating in chickens.[/h] Youk SS[SUP]1[/SUP], Lee DH[SUP]1,[/SUP][SUP]2[/SUP], Leyson CM[SUP]1[/SUP], Smith D[SUP]1[/SUP], Criado MF[SUP]1[/SUP], DeJesus E[SUP]1,[/SUP][SUP]3[/SUP], Swayne DE[SUP]1[/SUP], Pantin-Jackwood MJ[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Outbreaks of highly pathogenic avian influenza (HPAI) virus subtype H7N3 have been occurring in commercial chickens in Mexico since its first introduction in 2012. In order to determine changes in virus pathogenicity and adaptation in avian species, three H7N3 HPAI viruses from 2012, 2015, and 2016 were evaluated in chickens and mallards. All three viruses caused high mortality in chickens when given at medium to high doses and replicated similarly. No mortality or clinical signs and similar infectivity were observed in mallards inoculated with the 2012 and 2016 viruses. However, the 2012 H7N3 HPAI virus replicated well in mallards and transmitted to contacts, whereas the 2016 virus replicated poorly and did not transmit to contacts, which indicates that the 2016 virus is less adapted to mallards. In vitro, the 2016 virus grew slower and to lower titers than the 2012 virus in duck fibroblast cells. Full genome sequencing showed 115 amino acid differences between the 2012 and the 2016 virus, with some of these changes previously associated with changes in replication in avian species including HA A125T, NP M105V and NP S377N. In conclusion, as the Mexican H7N3 HPAI virus has passaged through large populations of chickens in a span of several years, it has retained its high pathogenicity for chickens but has decreased in fitness in mallards which could limit the potential spread of this HPAI virus by waterfowl.ImportanceNot much is known about changes in host adaptation of avian influenza (AI) viruses in birds after long-term circulation in chickens or other terrestrial poultry. Although the origin of AI viruses affecting poultry is wild aquatic birds, the role of these later birds in further dispersal of poultry-adapted AI viruses is not clear. Previously, we showed that HPAI viruses isolated early from poultry outbreaks could still infect and transmit well in mallards. In this study, we demonstrate that the Mexican H7N3 HPAI virus after four years of circulation in chickens replicates poorly and does not transmit in mallards, but still remains highly pathogenic in chickens. This information on changes in host adaptation is important for understanding the epidemiology of AI viruses and the role that wild waterfowl may play in disseminating viruses adapted to terrestrial poultry.
This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.
PMID: 31068421 DOI: 10.1128/JVI.00543-19
[h=1]Loss of fitness in mallards of Mexican H7N3 highly pathogenic avian influenza virus after circulating in chickens.[/h] Youk SS[SUP]1[/SUP], Lee DH[SUP]1,[/SUP][SUP]2[/SUP], Leyson CM[SUP]1[/SUP], Smith D[SUP]1[/SUP], Criado MF[SUP]1[/SUP], DeJesus E[SUP]1,[/SUP][SUP]3[/SUP], Swayne DE[SUP]1[/SUP], Pantin-Jackwood MJ[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Outbreaks of highly pathogenic avian influenza (HPAI) virus subtype H7N3 have been occurring in commercial chickens in Mexico since its first introduction in 2012. In order to determine changes in virus pathogenicity and adaptation in avian species, three H7N3 HPAI viruses from 2012, 2015, and 2016 were evaluated in chickens and mallards. All three viruses caused high mortality in chickens when given at medium to high doses and replicated similarly. No mortality or clinical signs and similar infectivity were observed in mallards inoculated with the 2012 and 2016 viruses. However, the 2012 H7N3 HPAI virus replicated well in mallards and transmitted to contacts, whereas the 2016 virus replicated poorly and did not transmit to contacts, which indicates that the 2016 virus is less adapted to mallards. In vitro, the 2016 virus grew slower and to lower titers than the 2012 virus in duck fibroblast cells. Full genome sequencing showed 115 amino acid differences between the 2012 and the 2016 virus, with some of these changes previously associated with changes in replication in avian species including HA A125T, NP M105V and NP S377N. In conclusion, as the Mexican H7N3 HPAI virus has passaged through large populations of chickens in a span of several years, it has retained its high pathogenicity for chickens but has decreased in fitness in mallards which could limit the potential spread of this HPAI virus by waterfowl.ImportanceNot much is known about changes in host adaptation of avian influenza (AI) viruses in birds after long-term circulation in chickens or other terrestrial poultry. Although the origin of AI viruses affecting poultry is wild aquatic birds, the role of these later birds in further dispersal of poultry-adapted AI viruses is not clear. Previously, we showed that HPAI viruses isolated early from poultry outbreaks could still infect and transmit well in mallards. In this study, we demonstrate that the Mexican H7N3 HPAI virus after four years of circulation in chickens replicates poorly and does not transmit in mallards, but still remains highly pathogenic in chickens. This information on changes in host adaptation is important for understanding the epidemiology of AI viruses and the role that wild waterfowl may play in disseminating viruses adapted to terrestrial poultry.
This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.
PMID: 31068421 DOI: 10.1128/JVI.00543-19