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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #302458
Title: Immune response to influenza A virus hemagglutinin protein is sufficient to induce vaccine-associated enhanced respiratory disease

Author
item RAJÃO, DANIELA - Non ARS Employee
item Loving, Crystal
item GAUGER, PHILLIP - Iowa State University
item Kitikoon, Pravina
item Baker, Amy

Submitted to: American Society for Virology Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 4/14/2014
Publication Date: 6/21/2014
Citation: Rajão, D.S., Loving, C.L., Gauger, P.C., Kitikoon, P., Vincent, A.L. 2014. Immune response to influenza A virus hemagglutinin protein is sufficient to induce vaccine-associated enhanced respiratory disease. American Society for Virology 33rd Annual Meeting. p. 199.

Interpretive Summary:

Technical Abstract: The antigenic diversity of influenza A virus (IAV) circulating in pigs continues to complicate control of swine influenza through the use of vaccination in the United States. The antibody response elicited by whole inactivated virus (WIV) vaccines can lead to vaccine-associated enhanced respiratory disease (VAERD) when pigs are challenged with heterologous virus. The aim of this study was to compare the effects of heterologous delta1-H1N2 IAV challenge after vaccination of pigs with 2009 pandemic H1N1 virus (H1N1pdm09) recombinant hemagglutinin (HA) subunit vaccine (HA-SV) or temperature-sensitive live attenuated influenza virus (LAIV) vaccine, and to assess the role of immunity to HA in the development of VAERD. Both HA-SV and LAIV vaccines induced high neutralizing antibodies to virus with homologous HA (H1N1pdm09), but not to the heterologous challenge virus (delta1-H1N2). No virus was detected in the lungs of LAIV vaccinated pigs by 5 days post infection (dpi) and pigs in this group had reduced virus titers in nasal secretions, indicating partial protection. HA-SV vaccinated pigs developed more severe lung and tracheal lesions following challenge, consistent with VAERD, however at an intermediate level than previously observed with WIV vaccination. These results demonstrate that immunity to IAV HA protein alone was sufficient to initiate the mechanisms involved with VAERD following heterologous challenge, but immune response to other viral proteins may be involved in the magnitude of the immunopathology seen with WIV.