|YOUK, SUNG-SU - Orise Fellow|
|LEE, DONG-HUN - Orise Fellow|
|LEYSON, CHRISTINA - Orise Fellow|
|FERREIRA CRIADO, MIRIA - Orise Fellow|
Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/30/2019
Publication Date: 6/28/2019
Citation: Youk, S., Lee, D., Leyson, C., Smith, D.M., Ferreira Criado, M., Dejesus, E.G., Swayne, D.E., Pantin Jackwood, M.J. 2019. Loss of fitness of Mexican H7N3 highly pathogenic avian influenza virus in mallards after circulating in chickens. Journal of Virology. 93(14):e00543-19. https://doi.org/10.1128/JVI.00543-19.
Interpretive Summary: Avian influenza (AI) continues to be a threat to poultry worldwide. Highly pathogenic avian influenza (HPAI) of the subtype H7N3 continues to cause outbreaks in Mexico. In this study we examine the infectivity and transmissibility of 2012, 2015, and 2016 Mexican H7N3 HPAI viruses in chickens. No differences were found between the viruses, all three caused high mortality in chickens. In order to address the role of waterfowl in the spread of H7N3 viruses, the infectivity and transmissibility of the 2012 and 2016 viruses was examined in mallards. The 2012 H7N3 virus infected all mallards when given a medium and high doses and the virus transmitted to all contacts in these groups. The more recent 2016 Mexican HPAI virus replicated poorly and didn’t transmit to contacts, indicating this virus was less adapted to mallards. No virus-infected mallards showed clinical signs or died. In conclusion, as the H7N3 HPAI virus has passed in chickens, it has decreased in adaptation to mallards remaining highly lethal to chickens. We speculate that this adaptation possibly could limit any potential spread of this HPAI virus by waterfowl.
Technical Abstract: 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 did the 2012 virus in duck fibroblast cells. Full-genome sequencing showed 115 amino acid differences between the 2012 and the 2016 viruses, with some of these changes previously associated with changes in replication in avian species, including hemagglutinin (HA) A125T, nucleoprotein (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 and has retained its high pathogenicity for chickens, it has decreased in fitness in mallards, which could limit the potential spread of this HPAI virus by waterfowl.