|YOUK, SONGSU - Orise Fellow|
|LEE, DONG-HUN - University Of Connecticut|
|KILLIAN, MARY - Animal And Plant Health Inspection Service (APHIS)|
|TORCHETTI, MIA - Animal And Plant Health Inspection Service (APHIS)|
Submitted to: Emerging Infectious Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/21/2020
Publication Date: 12/15/2020
Citation: Youk, S., Lee, D., Killian, M.L., Pantin Jackwood, M.J., Swayne, D.E., Torchetti, M.K. 2020. High pathogenicity avian influenza A(H7N3) virus in poultry, United States, 2020. Emerging Infectious Diseases. 26(12):2966-2969. https://doi.org/10.3201/eid2612.202790.
Interpretive Summary: High pathogenicity avian influenza viruses (HPAIV) have devastating impacts on the poultry industries. In March 2020, an outbreak of H7N3 low pathogenicity avian influenza (LPAIV) occurred in 9 turkey farms in North Carolina (NC) and a farm in South Carolina (SC). A in a second turkey farm in SC, with increased mortality and respiratory signs, a H7N3 HPAIV was detected. The virus mutated to the highly pathogenic form via a 27-nucleotide host cellular 28S rRNA insertion in the hemagglutinin (HA) gene. All the premises affected by H7N3 LPAIV and HPAIV were located in three adjacent counties, one across state lines, indicating that geographical proximity was relevant to the outbreaks. Immediate depopulation was performed on affected premises for a total of 361,000 birds. Complete genome sequencing and phylogenetic analyses indicated the wild bird origin of the H7N3 viruses. The H7 HA genes of recent U.S. poultry events (2016, 2017, and 2020) originate from the same North American wild bird H7 clade. With several recent incursions, this H7 HA clade represents a repetitive threat to domestic poultry and carries with it the potential to mutate to HPAIV.
Technical Abstract: An outbreak of low-pathogenicity avian influenza A(H7N3) virus of North American wild bird lineage occurred on commercial turkey farms in North Carolina and South Carolina, USA, during March–April 2020. The virus mutated to the highly pathogenic form in 1 house on 1 farm via recombination with host 28S rRNA.