Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract only
Publication Acceptance Date: 11/11/2001
Publication Date: 11/11/2001
Citation: Interpretive Summary:
Technical Abstract: Swine influenza (SI) is an acute respiratory disease of swine caused by type A influenza viruses. Before 1998, mainly H1N1 SI viruses (SIV) were isolated from swine in the U.S. Since then antigenetically distinct reassortant H3N2 SIVs were identified as causative agents of respiratory disease in pigs on U.S. farms. The H3N2 SIVs currently circulating in the U.S. swine populations are triple reassortant viruses containing avian-, swine- and human-like gene segments. Recent sequence data revealed that the triple reassortant SIVs acquired at least three distinct H3 molecules from human influenza viruses, allowing a differentiation into three distinct antigenic clusters (I-III). One objective of the present study was to determine whether hyperimmune sera obtained from pigs, experimentally infected with selected viruses from each H3N2 cluster, showed cross-reactivity against the other cluster viruses by hemagglutination inhibition and neutralization tests. These in vitro studies revealed that H3N2 clusters I and III share common epitopes, whereas only limited cross-reactivity was observed with a cluster II H3N2 virus. Furthermore, seronegative pigs were intratracheally infected with various doses of selected SIVs from all three H3N2 clusters and monitored for clinical signs, virus replication and lesions in the respiratory tract. Particular H3N2 SIVs from each of the three clusters were able to induce clinical signs and associated lesions. Gross lesions in the lungs of infected pigs correlated with clinical signs and histopathological changes. Our in vivo studies provide the basis for future cross protection experiments in order to assess the efficacy of vaccines against circulating H3N2 SIV strains.