Submitted to: PLoS One
Publication Type: Peer reviewed journal
Publication Acceptance Date: 12/2/2010
Publication Date: 1/1/2011
Publication URL: http://handle.nal.usda.gov/10113/60740
Citation: Costa, T., Brown, J., Howerth, E.W., Stallknecht, D.E., Swayne, D.E. 2011. Homo- and heterosubtypic low pathogenic avian influenza exposure on H5N1 highly pathogenic avian influenza virus infection in wood ducks (Aix sponsa). PLoS One. 6(1):e15987. Interpretive Summary: Wild water birds can be a natural source of low pathogenicity avian influenza (LPAI) viruses. The impact of infections and antibodies from such infections on protection from high pathogenicity avian influenza viruses (HPAI) are unknown. In this study, we exposed wood ducks to several different H5N1 and H5N2 LPAI viruses before challenge with H5N1 HPAI virus. A LPAI virus pre-exposure did not prevent wood ducks from infection with and shedding of the H5N1 HPAI virus, but decreased the mortality rate and increased the mean time to death after HPAI challenge. These observations suggest that in natural occurring HPAI outbreaks, birds with pre-existing immunity to LPAI viruses can provide some protection but no completely prevent infection and death.
Technical Abstract: Wild birds in the Orders Anseriformes and Charadriiformes are the natural reservoirs for avian influenza (AI) viruses. Although they are often infected with multiple AI viruses, the significance and extent of acquired immunity in these populations is not understood. Pre-existing immunity to AI virus has been shown to modulate the outcome of a highly pathogenic avian influenza (HPAI) virus infection in multiple domestic avian species, but few studies have addressed this effect in wild birds. In this study, the effect of pre-exposure to homosubtypic (hemagglutinin homologous) and heterosubtypic (hemagglutinin heterologous) low pathogenic avian influenza (LPAI) viruses on the outcome of a H5N1 HPAI virus infection in Wood Ducks (Aix sponsa) was evaluated. A LPAI virus pre-exposure did not prevent wood ducks from infection with and shedding of the H5N1 HPAI virus, but decreased the mortality rate and increased the mean time to death after HPAI challenge. The magnitude of this effect on the outcome of the HPAI virus infection varied between LPAI viruses, and was associated with efficient LPAI viral replication and the development of a humoral immune response. These observations suggest that in natural occurring HPAI outbreaks, birds with pre-existing immunity to AI with homologous hemagglutinin or neuraminidase may either survive the HPAI infection or live longer than naïve birds, potentially posing a greater risk for contributing to viral transmission and dissemination. The mechanisms responsible for this protection and the duration of this protective immunity remain unknown. The results of this study are important for surveillance efforts and help clarify epidemiological data from outbreaks in wild bird populations.