Genetic Characterization of H3N2 Influenza Viruses Isolated from Pigs in North America, 1977–1999: Evidence for Wholly Human and Reassortant Virus Genotypes

Authors

Alexander I. Karasin, Uni6ersity of Wisconsin — Madison
Melissa M. Schutten, Uni6ersity of Wisconsin — Madison
Lynn A. Cooper, Influenza Branch, Centers for Disease Control and Pre6ention, 1600 Clifton Road, Atlanta, GA
Catherine B. Smith, Influenza Branch, Centers for Disease Control and Pre6ention, 1600 Clifton Road, Atlanta, GA
Kanta Subbarao, Influenza Branch, Centers for Disease Control and Pre6ention, 1600 Clifton Road, Atlanta, GA
Gary A. Anderson, ImmTech Biologics, LLC, 8600 West 239th Street, Bucyrus, KS 66013, USA
Suzanne Carman, Animal Health Laboratory, Uni6ersity of Guelph, Box 3612, Guelph, Ont., Canada N1H
Christopher W. Olsen, Uni6ersity of Wisconsin — Madison

Date of this Version

2000

Comments

Published in Virus Research 68 (2000) 71–85.

Abstract

Since 1998, H3N2 viruses have caused epizootics of respiratory disease in pigs throughout the major swine production regions of the U.S. These outbreaks are remarkable because swine influenza in North America had previously been caused almost exclusively by H1N1 viruses. We sequenced the full-length protein coding regions of all eight RNA segments from four H3N2 viruses that we isolated from pigs in the Midwestern U.S. between March 1998 and March 1999, as well as from H3N2 viruses recovered from a piglet in Canada in January 1997 and from a pig in Colorado in 1977. Phylogenetic analyses demonstrated that the 1977 Colorado and 1997 Ontario isolates are wholly human influenza viruses. However, the viruses isolated since 1998 from pigs in the Midwestern U.S. are reassortant viruses containing hemagglutinin, neuraminidase and PB1 polymerase genes from human influenza viruses, matrix, non-structural and nucleoprotein genes from classical swine viruses, and PA and PB2 polymerase genes from avian viruses. The HA proteins of the Midwestern reassortant swine viruses can be differentiated from those of the 1995 lineage of human H3 viruses by 12 amino acid mutations in HA1. In contrast, the Sw:ONT:97 virus, which did not spread from pig-to-pig, lacks 11 of these changes.