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Journal of Clinical Microbiology, May 2003, p. 1936-1941, Vol. 41, No. 5
0095-1137/03/$08.00+0     DOI: 10.1128/JCM.41.5.1936-1941.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Comparison of the Pathogenesis of Two Genetically Different H3N2 Influenza A Viruses in Pigs

Gabriele A. Landolt, Alexander I. Karasin, Lynette Phillips, and Christopher W. Olsen*

Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin—Madison, Madison, Wisconsin

Received 23 July 2002/ Returned for modification 17 December 2002/ Accepted 9 February 2003

In 1997 and 1998, H3N2 influenza A viruses emerged among pigs in North America. Genetic analyses of the H3N2 isolates demonstrated that they had distinctly different genotypes. The most commonly isolated viruses in the United States have a triple-reassortant genotype, with the hemagglutinin, neuraminidase, and PB1 polymerase genes being of human influenza virus origin, the nucleoprotein, matrix, and nonstructural genes being of classical swine influenza virus origin, and the PA and PB2 polymerase genes being of avian influenza virus origin. In contrast, a wholly human H3N2 virus was isolated from a single baby pig in Ontario, Canada, in 1997, but it did not spread within the swine population. Genetic differences between this wholly human virus and the triple-reassortant viruses may affect their replication efficiencies in pigs. In the present study we compared the pathogenicities and replication kinetics of the wholly human virus and a triple-reassortant virus in 7-week-old pigs that were infected intranasally with 2 x 103 to 2 x 106 50% tissue culture infective doses of virus. Our results demonstrate that the wholly human virus replicated to significantly lower titers and that the onset of virus shedding was delayed compared to the replication titers and the time of onset of virus shedding in triple-reassortant viruses. In addition, infection with the triple-reassortant virus was associated with moderate to severe gross pathological and histological pulmonary lesions, while infection with the wholly human virus induced only mild pulmonary changes.

* Corresponding author. Mailing address: Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin—Madison, 2015 Linden Dr., Madison, WI 53706. Phone: (608) 265-8681. Fax: (608) 263-0438. E-mail: olsenc{at}svm.vetmed.wisc.edu.

Journal of Clinical Microbiology, May 2003, p. 1936-1941, Vol. 41, No. 5
0095-1137/03/$08.00+0     DOI: 10.1128/JCM.41.5.1936-1941.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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