|Mccracken, Kevin - UNIV OF ALASKA-FAIRBANKS|
|Winker, Kevin - UNIV OF ALASKA-FAIRBANKS|
Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 9, 2006
Publication Date: July 13, 2006
Citation: Spackman, E., McCracken, K.G., Winker, K., Swayne, D.E. 2006. H7N3 avian influenza virus found in a South American wild duck is related to the Chilean 2002 poultry outbreak, contains genes from equine and North American wild bird lineages, and is adapted to domestic turkeys. Journal of Virology. 80(15):7760-7764. Interpretive Summary: Isolation of avian influenza virus (AIV) has never been reported from wild birds in South America, although AIV has been isolated from North American wild waterfowl for decades, minimal sampling has been done in South America. Wild waterfowl are the natural reservoir hosts for AIV and through migration may be able to disseminate the virus. Importantly commercial poultry, which are not natural hosts for the virus, are monitored for the virus, and it has only been confirmed once, in the outbreak Chile in 2002. A source of the virus was never found, but was assumed to be wild birds. Here we report a virus isolated from a cinnamon teal in Bolivia, which was collected in 2001, nearly 9 months prior to the outbreak in Chile. The virus was the same subtype as the virus from chickens and turkeys in Chile, however two of the eight gene segments were related to genes from North American isolates, indicating that there is some transfer of virus between North and South America. Finally, the virus was shown to be of the low pathogenic type, and appeared to be better adapted to turkeys, which were nearly 100,000 times more susceptible than chickens.
Technical Abstract: An H7N3 avian influenza virus (AIV) was isolated from a Cinnamon Teal (Anas Cyanoptera) (A/CinnamonTeal/Bolivia.4537/01) during a survey of wild waterfowl in Bolivia in 2001. The NA and M genes had the greatest identity with North American wild bird isolates, the NS was most closely related to an Equine virus and the remaining genes were most closely related to isolates from an outbreak of H7N3 in commercial chickens in Chile in 2002. The HA protein cleavage site and results of pathogenesis studies in chickens were consistent with a low pathogenicity virus and the infective dose was 100,000 times higher for chickens than turkeys.