|Linares, Jose - TX VET MED LAB-GONZALES|
|Senne, Dennis - NVSL - AMES, IA|
Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 31, 2005
Publication Date: September 1, 2005
Citation: Lee, C.W., Swayne, D.E., Linares, J.A., Senne, D.A., Suarez, D.L. 2005. H5N2 avian influenza outbreak in Texas in 2004: the first highly pathogenic strain in the United States in 20 years?. Journal of Virology. 79(17):11412-11421. Interpretive Summary: Avian influenza virus is found commonly in wild birds, and from this wild bird reservoir the virus can spread to poultry. There are many different groups of avian influenza, called subtypes. Although viruses from all the subtypes can cause some disease in chickens, the H5 and H7 subtypes of avian influenza cause the most concern because they can cause the most sever form of disease called highly pathogenic avian influenza. Highly pathogenic avian influenza spreads easily and can causes a high mortality in infected birds. Recently an outbreak of H5 influenza occurred in Texas. This virus was unique because it had some genetic features of a highly pathogenic virus, but it did not cause a high mortality in naturally or experimentally infected birds. Several studies were performed to understand why this virus did not cause disease where similar viruses did. The results showed that changes in the hemagglutinin gene could result in increased mortality. Fortunately the outbreak in Texas was identified and controlled quickly.
Technical Abstract: In early 2004, an H5N2 avian influenza (AI) virus that met the molecular criteria for classification as a high pathogenicity (HP) AI was isolated from the state of Texas in the United States. However, clinical manifestation of the affected flock was that of low pathogenicity (LP) AI and the representative virus was not virulent for experimentally inoculated chickens. The Texas/04 isolate had a similar hemagglutinin gene sequence as an H5N3 AI virus also isolated from chickens in Texas in 2002, but it had acquired one more basic amino acid at the cleavage site by a single point mutation. The isolate shared similar sequence with 2002 H5N3 virus in several internal genes, but some genes (PA, PB1 and PB2) had sequence of clearly different origin, which indicates the virus had undergone reassortment. The 2004 H5N2 isolate also had a stalk deletion in the N2 gene, characteristic of a chicken adapted AI virus. By analyzing viruses constructed by in vitro mutagenesis followed by reverse-genetics, we found that the pathogenicity of the virus could be increased in vitro and in vivo by the insertion of additional basic amino acid at the HA cleavage site and not by the loss of a glycosylation site near the cleavage site. Our study underscores the importance of continuing surveillance and control efforts regarding H5 and H7 subtype AI viruses in the United States.