|CHRZASTEK, KLAUDIA - ORISE FELLOW|
|SEGOVIA, KAREN - ORISE FELLOW|
|TORCHETTI, MIA - ANIMAL AND PLANT HEALTH INSPECTION SERVICE (APHIS)|
|KILLIAN, MARY - ANIMAL AND PLANT HEALTH INSPECTION SERVICE (APHIS)|
Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/7/2021
Publication Date: N/A
Interpretive Summary: Avian influenza viruses can be divided into highly pathogenic avian influenza (HPAI) viruses and low pathogenic avian influenza (LPAI) viruses. HPAI viruses are restricted to subtypes of H5 and H7 and cause severe illnesses in poultry species with high mortality rates, whereas LPAI viruses are typically maintained in waterfowl and can be transmitted to domestic poultry species resulting in subclinical infection or mild respiratory disease. After circulation in poultry species, some H5 and H7 LPAI viruses can mutate to HPAI form. In 2017, outbreaks of H7N9 LPAI virus and HPAI virus occurred at chicken poultry farms in Tennessee and were found in mixed species backyard farm and markets in Alabama, Kentucky and Georgia. This study aimed to characterize infection and transmissibility of a duck origin H7N9 isolate in chickens, to address the potential contribution of waterfowl in the spread of virus during the outbreak. The results demonstrate that infection resulted in all chickens developing viremia and transmitting virus to naive animals. In addition, this work support the potential transmission of LPAI and HAPI viruses from waterfowl to poultry.
Technical Abstract: In March 2017, isolation of both high pathogenic (HP) and low pathogenic (LP) avian influenza virus (AIV) were detected from poultry farms and backyard birds from several states in the southeast U.S. The isolations were sporadically intertwined implicating that a silent introduction of LPAIV had occurred in the region before the virus evolved into a HP form. Because the transmission of LPAIV from waterfowl to poultry is a known mechanism for evolution to HPAIV, we sought to characterize infection and transmission of a duck-origin H7N9 LPAIV in chickens and genetically compare this viral adaption to original H7N9-positive clinical field samples. Result of experimental infection demonstrated virus replication and transmission in chickens with overt clinical signs of disease, including shedding through both oral and cloacal routes. Unexpectedly, higher levels of virus shedding were observed in some cloacal swabs. Next generation sequence (NGS) analysis identified numerous non-synonymous mutations at the consensus level in the polymerase genes (PA, PB1, PB2) and hemagglutinin (HA) receptor binding site in challenge virus recovered from chickens, indicating virus adaption in a new host. Sequence analysis of clinical samples obtained during the outbreak containing both high and low pathogenic viruses identified few polymorphisms based on percent frequency, possibly implicating successful adaption of the virus to its host. Interestingly, many clinical samples with LPAIV contained low depth of coverage compared to the HPAIV samples, indicating lower levels of virus titers. Taken together, this work demonstrates that these H7N9 viruses may readily jump between species and were highly infectious in chickens, which may have contributed to its spread in the region and possibly to the transition to HP form.