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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #250776
Title: Efficacy of Inactivated Swine Influenza Virus Vaccines Against 2009 H1N1 Influenza Virus in Pigs

Author
item Baker, Amy
item CIACCI-ZANELLA, JANICE - Labex - Embrapa
item GAUGER, PHILIP - Iowa State University
item ZANELLA, ERALDO - Universidad De Passo Fundo
item Kehrli Jr, Marcus
item JANKE, BRUCE - Iowa State University
item Lager, Kelly

Submitted to: International Pig Veterinary Society (IPVS)
Publication Type: Proceedings
Publication Acceptance Date: 3/30/2010
Publication Date: 7/18/2010
Citation: Vincent, A.L., Ciacci-Zanella, J.R., Lorusso, A., Gauger, P.C., Zanella, E.R., Kehrli, Jr., M.E., Janke, B.H., Lager, K.M. 2010. Efficacy of Inactivated Swine Influenza Virus Vaccines Against 2009 H1N1 Influenza Virus in Pigs. In: Proceedings of the International Pig Veterinary Society Congress, July 18-21, 2010, Vancouver, Canada. p. 299.

Interpretive Summary:

Technical Abstract: Introduction. The gene constellation of the 2009 pandemic H1N1 virus is a unique combination from swine influenza A viruses (SIV) of North American and Eurasian lineages, but prior to April 2009 had never before been identified in swine or other species (1). Although its hemagglutinin gene is related to North American H1 SIV, it is unknown if vaccines currently used in U.S. swine would cross-protect against infection with pandemic H1N1. The objective of this study was to evaluate the efficacy of inactivated vaccines prepared with U.S. swine influenza viruses as well as an experimental homologous H1N1 vaccine to prevent infection and disease from 2009 pandemic H1N1. Materials and methods. Sixty three-week-old cross-bred pigs were obtained from a herd free of SIV and porcine reproductive and respiratory syndrome virus (PRRSV). A/California/04/2009 H1N1 (CA/09) was propagated in Madin-Darby Canine Kidney (MDCK) cells for use in the study described below. Three inactivated vaccines (Vaccines A, B, and D) were selected based on serologic evidence of cross-reactivity in a previous study(2). Commercial vaccines were supplied by the manufacturers for use in the study and administered as per label. Vaccine A (FluSure® XP, Pfizer Animal Health, New York, NY) is a fully licensed trivalent commercial product containing cluster IV H3N2, gamma-cluster H1N1, and delta-cluster H1N1 SIV as vaccine seed viruses. Vaccine B (MaxiVac Excell® 5.0, Intervet/Schering-Plough, Boxmeer, The Netherlands) is a pentavalent product containing clusters I and IV H3N2 and Beta-, gamma-, and delta-cluster H1 SIV as vaccine seed viruses. Vaccine D (Newport Labs, Worthington, MN) is a bivalent autogenous vaccine containing Beta- and gamma-cluster H1 SIV as vaccine seed viruses. A monovalent experimental vaccine (Vaccine E) was prepared from CA/09 at 8 HA units per 50 uL and 1 X 10**6.5 50% tissue culture infectious dose (TCID50) per mL with inactivation by ultraviolet irradiation and addition of a commercial adjuvant. Pigs (N=10 per group) were vaccinated with 2 mL of each vaccine by the intramuscular route at approximately 4 weeks of age, boosted at 7 weeks of age, and challenged at 10 weeks of age. Nasal swabs were taken at 0, 3, and 5 days post infection (dpi). At necropsy, lungs were removed to estimate the percentage of macroscopic pneumonia. Each lung was lavaged to obtain bronchoalveolar fluid (BALF). Virus titers in BALF were determined by serial dilutions added to MDCK cells in 96-well plates, and virus from nasal swab samples were isolated on MDCK cells in 48-well plates and positive samples titrated in 96-well plates. Hemagglutination inhibition (HI) assays were done to evaluate sero-conversion using challenge virus as well as a panel of North American H1 SIV isolates representing each phylogenetic cluster (3). Results. All vaccines tested provided partial protection ranging from reduction of pneumonia lesions to significant reduction in virus replication in the lung and nose. Although the multivalent vaccines demonstrated partial protection, none were able to prevent all nasal shedding or clinical disease. An experimental homologous 2009 H1N1 monovalent vaccine provided optimal protection with no virus detected from nose or lung at any time point in addition to amelioration of clinical disease. The CA/09 vaccine induced high HI titers against 2009 H1N1 as well as cross-reacting HI antibodies against alpha-, Beta-, and gamma-cluster H1N1. Commercial vaccines that induced gamma-cluster HI antibodies demonstrated statistically significant reduction in virus titers. Discussion. Based on cross-protection demonstrated with the vaccines evaluated in this study, the U.S. swine herd likely has significant immunity to 2009 H1N1 from prior vaccination or natural exposure, especially those demonstrating immunity against gamma-clust