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Journal of Virology, September 2005, p. 11412-11421, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11412-11421.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

H5N2 Avian Influenza Outbreak in Texas in 2004: the First Highly Pathogenic Strain in the United States in 20 Years?

Chang-Won Lee,1 David E. Swayne,1 Jose A. Linares,2 Dennis A. Senne,3 and David L. Suarez1*

Southeast Poultry Research Laboratory, USDA Agricultural Research Service, Athens, Georgia 30605,1 Texas Veterinary Medical Diagnostic Laboratory, Poultry Diagnostic Laboratory, Gonzales, Texas 78629,2 National Veterinary Services Laboratories, USDA Animal and Plant Health Inspection Service, Ames, Iowa 500103

Received 9 February 2005/ Accepted 27 May 2005

In early 2004, an H5N2 avian influenza virus (AIV) that met the molecular criteria for classification as a highly pathogenic AIV was isolated from chickens in the state of Texas in the United States. However, clinical manifestations in the affected flock were consistent with avian influenza caused by a low-pathogenicity AIV and the representative virus (A/chicken/Texas/298313/04 [TX/04]) was not virulent for experimentally inoculated chickens. The hemagglutinin (HA) gene of the TX/04 isolate was similar in sequence to A/chicken/Texas/167280-4/02 (TX/02), a low-pathogenicity AIV isolate recovered from chickens in Texas in 2002. However, the TX/04 isolate had one additional basic amino acid at the HA cleavage site, which could be attributed to a single point mutation. The TX/04 isolate was similar in sequence to TX/02 isolate in several internal genes (NP, M, and NS), but some genes (PA, PB1, and PB2) had sequence of a clearly different origin. The TX/04 isolate also had a stalk deletion in the NA gene, characteristic of a chicken-adapted AIV. By analyzing viruses constructed by in vitro mutagenesis followed by reverse genetics, we found that the pathogenicity of the TX/04 virus could be increased in vitro and in vivo by the insertion of an additional basic amino acid at the HA cleavage site and not by the loss of a glycosylation site near the cleavage site. Our study provides the genetic and biologic characteristics of the TX/04 isolate, which highlight the complexity of the polygenic nature of the virulence of influenza viruses.

* Corresponding author. Mailing address: Southeast Poultry Research Laboratory, USDA-ARS, 934 College Station Road, Athens, GA 30605. Phone: (706) 546-3479. Fax: (706) 546-3161. E-mail: dsuarez{at}seprl.usda.gov.

Journal of Virology, September 2005, p. 11412-11421, Vol. 79, No. 17
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.17.11412-11421.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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