Submitted to: Pig Veterinary Society International Congress Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 6/3/2002
Publication Date: 6/3/2002
Citation: N/A 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 have been identified as causative agents of respiratory disease in pigs on U.S. farms. The H3N2 SIVs are triple reassortant viruses containing avian-, swine- and human-like gene segments These triple reassortant SIVs acquired at least 3 distinct H3 molecules from human influenza viruses allowing a differentiation into 3 distinct antigenic clusters (I-III). In vitro studies using hyperimmune sera obtained from CDCD pigs revealed that H3N2 clusters I and III share common epitopes, whereas only limited cross-reactivity was observed with a cluster II H3N2 virus. Intratracheal infection of pigs with selected SIVs from all three H3N2 clusters resulted in clinical signs and associated lesions; however, there were differences in severity of clinical signs and lesions between individual strains even within one antigenic cluster. These studies provide the basis for future cross protection experiments in order to assess the efficacy of vaccines against circulating H3N2 SIV strains. In addition, in vitro and in vivo studies were conducted using plasmid-derived double and triple reassortant H3N2 viruses which were obtained using a DNA transfection system for the generation of influenza A viruses from eight plasmids. Parental and plasmid-derived H3N2 viruses showed similar in vitro growth characteristics and in vivo pathogenicity. The advent of the SIV reverse genetics system will allow us to generate and manipulate any swine influenza virus and study the molecular basis of their pathogenicity and host-range restriction in its natural host, the pig.