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Lack of chicken adaptation of newly emergent Eurasian H5N8 and reassortant H5N2 high pathogenicity avian influenza viruses in the U.S. is consistent with restricted poultry outbreaks in the Pacific flyway during 2014–2015

Kateri Bertran, David E. Swayne, Mary J. Pantin-Jackwood, Darrell R. Kapczynski, Erica Spackman, David L. Suarez
Virology 2016 v.494 pp. 190-197
Influenza A virus, avian influenza, chickens, death, disease outbreaks, disease transmission, endothelial cells, models, pathogenesis, pathogenicity, seroconversion, virus replication, viruses, wild birds, United States
In 2014–2015, the U.S. experienced an unprecedented outbreak of Eurasian clade H5 highly pathogenic avian influenza (HPAI) virus, initially affecting mainly wild birds and few backyard and commercial poultry premises. To better model the outbreak, the pathogenesis and transmission dynamics of representative Eurasian H5N8 and reassortant H5N2 clade HPAI viruses detected early in the North American outbreak were investigated in chickens. High mean chicken infectious doses and lack of seroconversion in survivors indicated the viruses were poorly chicken adapted. Pathobiological features were consistent with HPAI virus infection, although the delayed appearance of lesions, longer mean death times, and reduced replication in endothelial cells differed from features of most other Eurasian H5N1 HPAI viruses. Although these initial U.S. H5 HPAI viruses had reduced adaptation and transmissibility in chickens, multi-generational passage in poultry could generate poultry adapted viruses with higher infectivity and transmissibility.