Seasonal Trivalent Inactivated Influenza Vaccine Does Not Protect against Newly Emerging Variants of Influenza A (H3N2v) Virus in Ferrets

Influenza Division, National Center for Immunization and Respiratory Diseases, Center for Disease Control and Prevention, Atlanta, GA 30333.
Journal of Virology (Impact Factor: 4.44). 10/2012; 87(2). DOI: 10.1128/JVI.02625-12
Source: PubMed


The recent increase in human cases of influenza A H3N2 variant virus [A(H3N2)v] highlights the need to assess whether seasonal
influenza vaccination provides cross-protection against A(H3N2)v virus. Our data demonstrate that the 2011-2012 trivalent
inactivated influenza vaccine (TIV) protected ferrets against homologous H3N2 virus challenge but provided minimal to no protection
against A(H3N2)v virus. The complete absence of specific hemagglutination inhibition antibody response to A(H3N2)v is consistent
with the poor cross-protection observed among TIV-immune animals.

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    • "These results are similar to those previously described for ferrets infected with H1N1pdm09 and seasonal viruses [32]–[34]. Although the clinical protection conferred by TIV was modest, it is similar to that previously described for ferrets vaccinated with TIV [35]. "
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    ABSTRACT: Ferrets are a useful animal model for human influenza virus infections, since they closely mimic the pathogenesis of influenza viruses observed in humans. However, a lack of reagents, especially for flow cytometry of immune cell subsets, has limited research in this model. Here we use a panel of primarily species cross-reactive antibodies to identify ferret T cells, cytotoxic T lymphocytes (CTL), B cells, and granulocytes in peripheral blood. Following infection with seasonal H3N2 or H1N1pdm09 influenza viruses, these cell types showed rapid and dramatic changes in frequency, even though clinically the infections were mild. The loss of B cells and CD4 and CD8 T cells, and the increase in neutrophils, were especially marked 1-2 days after infection, when about 90% of CD8+ T cells disappeared from the peripheral blood. The different virus strains led to different kinetics of leukocyte subset alterations. Vaccination with homologous vaccine reduced clinical symptoms slightly, but led to a much more rapid return to normal leukocyte parameters. Assessment of clinical symptoms may underestimate the effectiveness of influenza vaccine in restoring homeostasis.
    Full-text · Article · Jun 2014 · PLoS ONE
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    Full-text · Conference Paper · Jan 2013
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    ABSTRACT: The demonstrated link between the emergence of H3N2 variant (H3N2v) influenza A viruses (IAVs) and swine exposure at agricultural fairs has raised concerns about the human health risk posed by IAV-infected swine. Understanding the antigenic profiles of IAVs circulating in pigs at agricultural fairs is critical to developing effective prevention and control strategies. Here 68 H3N2 IAV isolates recovered from pigs at Ohio fairs (2009 to 2011) were antigenically characterized. These isolates were compared with other H3 IAVs recovered from commercial swine, wild birds, and canines, along with human seasonal and variant H3N2 IAVs. Antigenic cartography demonstrated that H3N2 IAV isolates from Ohio fairs could be divided into two antigenic groups: 1) the 2009 fair isolates and 2) the 2010 and 2011 fair isolates. These same two antigenic clusters have also been observed in commercial swine populations in recent years. Human H3N2v isolates from 2010 and 2011 are antigenically clustered with swine-origin IAVs from the same time period. The isolates recovered from pigs at fairs did not cross react with ferret antisera produced against the human seasonal H3N2 IAVs circulating during the past decade, raising the question of the degree of immunity the human population has to swine-origin H3N2 IAVs. Our results demonstrate that H3N2 IAVs infecting pigs at fairs and H3N2v isolates were antigenically similar to the IAVs circulating in commercial swine, demonstrating that exhibition swine can function as a bridge between commercial swine and the human population.
    Full-text · Article · May 2013 · Journal of Virology
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