|Janke, Bruce - IOWA STATE UNIVERSITY|
|Woods, Roger - ARS-RETIRED|
|Webster, Robert - ST JUDE, MEMPHIS, TN|
|Webby, Richard - ST JUDE, MEMPHIS, TN|
Submitted to: Journal of Clinical Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 28, 2003
Publication Date: July 1, 2003
Citation: RICHT, J., LAGER, K.M., JANKE, B.H., WOODS, R.D., WEBSTER, R.G., WEBBY, R.J. PATHOGENIC AND ANTIGENIC PROPERTIES OF PHYLOGENETICALLY DISTINCT REASSORTANT H3N2 SWINE INFLUENZA VIRUSES CO-CIRCULATING IN THE UNITED STATES. JOURNAL OF CLINICAL MICROBIOLOGY. 2003. v. 41. p. 3198-3205. Interpretive Summary: Swine influenza (SI) is an acute respiratory disease of swine that is caused by swine influenza virus (SIV), a type A influenza virus. Swine and other mammalian and avian type A influenza virus subtypes can be differentiated one from another based on unique virus proteins present on the surface of each virus subtype. Before 1998, almost all SIV isolates in the United States were of the same subtype, the H1N1 subtype. This subtype was typically associated with respiratory disease in pigs during the grower or finisher stages of production. However, during 1998 a new SIV subtype, the H3N2 subtype, was isolated in the United States from epidemics of respiratory disease in fattening pigs and sows and abortions. Genetic analysis of these H3N2 virus isolates indicated that some were a combination of type A influenza viruses from birds, humans, and swine, and others were just a combination of avian and swine influenza virus subtypes. Summarized in this paper are studies with SIV H3N2 isolates, which were grouped into 3 additional categories referred to as clusters I, II, and III. When given to 4-week-old pigs, cluster I, II, or III H3N2 SIV subtypes caused them to become ill and develop respiratory disease. In contrast, when the same viruses were given to 12-week-old pigs, they were not as clinically affected. Additional studies indicate the cluster I and III viruses are much more closely related when compared to the cluster II virus. Collectively, these studies provide the basis for future cross protection experiments that can be used to assess the efficacy of new SIV vaccines.
Technical Abstract: Swine influenza is an acute respiratory disease caused by type A influenza viruses. Before 1998, swine influenza isolates in the U.S. were mainly of the classical H1N1 lineage. Since then, phylogenetically distinct reassortant H3N2 viruses have been identified as respiratory pathogens in pigs on U.S. farms. The H3N2 viruses currently circulating in the U.S. swine population are triple reassortants containing avian-like (PA, PB2), swine-like (M, NP, NS), and human-like (HA, NA, PB1) gene segments. Recent sequence data show that the triple reassortants have acquired at least three distinct H3 molecules from human influenza viruses and thus form three distinct phylogenetic clusters (I-III). In this study we analyzed the antigenic and pathogenic properties of viruses belonging to each of these clusters. Hemagglutination inhibition and neutralization assays using hyperimmune sera obtained from hysterectomy-derived, colostrum-deprived pigs, revealed that H3N2 clusters I and III viruses share common epitopes, whereas a cluster II virus showed only limited cross-reactivity. H3N2 viruses from each of the three clusters were able to induce clinical signs of disease and associated lesions upon intratracheal inoculation into seronegative pigs. There were, however, differences in the severity of lesions between individual strains even within one antigenic cluster. A correlation between the severity of disease and pig age was observed. These data highlight the increased diversity of swine influenza in the U.S. and would argue that surveillance should be intensified to determine the most suitable vaccine components.