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Title:   Author  item
                                            Baker, Amyitem
                                            Lager, Kellyitem
                                            GRAMER, MARIE - UNIVERSITY OF MINNESOTAitem
                                            Richt, Juergenitem
                                            JANKE, BRUCE - IOWA STATE UNIVERSITY
  Submitted to: International Pig Veterinary Society (IPVS)
                                    Publication Type: Proceedings
                                    Publication Acceptance Date: 4/10/2006
                                    Publication  Date: 7/16/2006
                                    Citation: Vincent, A.L., Lager, K.M., Gramer, M.G., Richt, J.A., Janke, B.H. 2006. Failure of cross-protection by inactivated vaccines for two U.S.  H1 swine influenza virus (SIV) isolates. In: Proceedings of the 19th International Pig Veterinary Society Congress, July 16-19, 2006, Copenhagen, Denmark. p. 266.Interpretive Summary:
                                Technical Abstract: Influenza in swine is an acute respiratory disease caused by influenza A viruses. Reassortant H1 viruses (rH1N1 and H1N2) are reported to be infecting and causing disease in herds that have been vaccinated with vaccines containing cH1N1, despite the observation that the hemagglutinin (HA) genes from the H1N2 and rH1N1 are of swine origin. In this study, we evaluated two U.S. SIV isolates, A/Swine/Iowa/15/1930 H1N1 (IA30) and A/Swine/Minnesota/00194/2003 H1N2 (MN03), with substantial genetic variation in the HA gene and failure to cross-react in the hemagglutination inhibition (HI) assay in an in vivo vaccination model. These isolates were utilized to prepare inactivated vaccines used to immunize conventional pigs at 3 and 6 weeks of age, followed by challenge with homologous or heterologous viruses at 8 weeks of age. Both inactivated vaccines provided excellent protection against homologous challenge. However, the IA30 vaccine failed to reduce virus shedding, virus titers in the lung, and lung lesions against the heterologous MN03 challenge. Surprisingly, 3 of the 8 pigs had substantially greater percentages of lung lesions. In addition, there is evidence which suggests the IA30 inactivated vaccine potentiated the level of pneumonia with the heterologous MN03 challenge, and this potentiation may have been immune-mediated due to the high levels of presumably non-neutralizing IgG antibodies in the lung of 3 of the 8 pigs. The IA30 challenge was mild and the MN03 vaccine provided partial protection against the heterologous IA30 challenge. The vaccines induced an isolate specific HI response with sufficient titers against homologous virus, but there was no cross-reactivity with heterologous viruses. Divergent H1 viruses that do not cross-react serologically may not provide complete cross-protection when used as an inactivated vaccine against heterologous challenge. Cross-protection does not appear to be bi-directional as the MN03 inactivated vaccine provided some protection against the IA30 challenge.


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