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United States Department of Agriculture

Agricultural Research Service

Title: Evolution of Avian Influenza in Gallinaceous Birds in the Live-Bird Market System of the U.S.

Authors
item Spackman, Erica
item Swayne, David
item Suarez, David

Submitted to: Proceedings of the Noble Foundation Workshop in Virus Evolution
Publication Type: Abstract Only
Publication Acceptance Date: October 1, 2004
Publication Date: October 22, 2004
Citation: Spackman, E., Swayne, D.E., Suarez, D.L. Evolution of Avian Influenza in Gallinaceous Birds in the Live-Bird Market System of the U.S. Virus Evolution Workshop, Noble Foundation, October 22, 2004, Ardmore, Oklahoma. p. 12.

Technical Abstract: Avian influenza virus (AIV) is type A influenza, which can replicate in a wide range of host species including both avians and mammals. However the natural host species for type A influenza are wild waterfowl and shorebirds. Because gallinaceous birds (chickens, turkeys and quail) are non-natural hosts the virus undergoes genetic changes to adapt to replication in these species. A rare example this is an H7N2 AIV lineage endemic to the live-bird market system (LBMS) in the North East U.S. for over 10 years. Importantly, the LBMS provides a unique environment for AIV evolution; 1) multiple avian and mammalian species are housed in close contact allowing for regular exposure of AIV from waterfowl to other species, 2) there is a constant influx of susceptible animals, and 3) bio-security is poor. Furthermore, due to numerous recent reports, from around the world, of direct transmission of AIV from poultry to humans, the importance of understanding the evolution of AIV in environments such as the LBMS is emphasized. Four genes from this AIV lineage, the hemagglutinin (HA), neuraminidase (NA), matrix (M) and non-structural (NS) genes, have been characterized from over 40 isolates since 1994. Several notable features have evolved and may be related to the apparent biological adaptation of these viruses to replication in poultry. The HA gene of these isolates has acquired a unique deletion in the receptor binding site that appears to be a novel mechanism for the virus to compensate for a deletion in the NA protein, a feature associated with poultry adapted AIV. Additionally, the HA, which is also the primary gene responsible for virus virulence, has acquired cumulative protein sequence changes consistent with a shift toward greater virulence. Phylogenetic analysis of the M and NS genes shows that these genes group separately from of those of their putative parental viruses from North American wild waterfowl. Importantly, genetic features that have previously been associated with the transmission of avian viruses to humans are absent from this lineage. A low rate of isolations of this lineage from waterfowl in the LBMS that cannot be explained by lack of exposure or sampling, suggests biological evidence that this lineage has adapted to poultry. Another interesting characteristic of these viruses is that the minimal infectious dose in chickens is 100 times greater than that for turkeys, demonstrating that important biological differences exist even among gallinaceous poultry in the virus-host interaction.

Last Modified: 10/24/2014
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