|BETRAN, KATERI - Consultant|
|CRIADO, MIRIA FERREIRA - Consultant|
|LEE, DONG-HUN - Orise Fellow|
Submitted to: Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/27/2019
Publication Date: 11/1/2019
Citation: Betran, K., Pantin Jackwood, M.J., Criado, M., Lee, D., Balzli, C.L., Spackman, E., Suarez, D.L., Swayne, D.E. 2019. Pathobiology and innate immune responses of gallinaceous poultry to clade 22.214.171.124A H5Nx highly pathogenic avian influenza virus infection. Veterinary Research. 50:89. https://doi.org/10.1186/s13567-019-0704-5.
Interpretive Summary: In the 2014-2015 highly pathogenic avian influenza (HPAI) outbreak in the U.S., backyard flocks of mixed poultry and large commercial chicken and turkey operations were affected. The disease caused by the first U.S. isolates was investigated in mixed species of poultry causing microscopic damage and high quantity of virus growth in severely ill birds. These changes were similar across all species of poultry. The HPAI virus infection was modulated in Japanese quail because of innate immune response.
Technical Abstract: In the 2014–2015 Eurasian lineage clade 126.96.36.199A H5 highly pathogenic avian influenza (HPAI) outbreak in the U.S., backyard flocks with minor gallinaceous poultry and large commercial poultry (chickens and turkeys) operations were affected. The pathogenesis of the first H5N8 and reassortant H5N2 clade 188.8.131.52A HPAI U.S. isolates was investigated in six gallinaceous species: chickens, Japanese quail, Bobwhite quail, Pearl guinea fowl, Chukar partridges, and Ring-necked pheasants. Both viruses caused 80–100% mortality in all species, except for H5N2 virus that caused 60% mortality in chickens. The surviving challenged birds remained uninfected based on lack of clinical disease and lack of seroconversion. Among the infected birds, chickens and Japanese quail in early clinical stages (asymptomatic and listless) lacked histopathologic findings. In contrast, birds of all species in later clinical stages (moribund and dead) had histopathologic lesions and systemic virus replication consistent with HPAI virus infection in gallinaceous poultry. These birds had widespread multifocal areas of necrosis, sometimes with heterophilic or lymphoplasmacytic inflammatory infiltrate, and viral antigen in parenchymal cells of most tissues. In general, lesions and antigen distribution were similar regardless of virus and species. However, endotheliotropism was the most striking difference among species, with only Pearl guinea fowl showing widespread replication of both viruses in endothelial cells of most tissues. The expression of IFN-' and IL-10 in Japanese quail, and IL-6 in chickens, were up-regulated in later clinical stages compared to asymptomatic birds.