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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #349412
Research Project: Intervention Strategies to Control Influenza A Virus Infection in Swine

Location: Virus and Prion Research

Title: The other influenza surface glycoprotein: probing the antigenic differences between N2 neuraminidase lineages of North American swine influenza a viruses

Author
item KAPLAN, BRYAN - Orise Fellow
item Anderson, Tavis
item SANTOS, JEFFERSON - University Of Georgia
item PEREZ, DANIEL - University Of Georgia
item LEWIS, NICOLA - Animal & Plant Health Agency Apha
item Baker, Amy

Submitted to: International Symposium on Neglected Influenza Viruses
Publication Type: Abstract Only
Publication Acceptance Date: 3/1/2018
Publication Date: 4/18/2018
Citation: Kaplan, B.S., Anderson, T.K., Santos, J., Perez, D., Lewis, N., Vincent, A.L. 2018. The other influenza surface glycoprotein: probing the antigenic differences between N2 neuraminidase lineages of North American swine influenza a viruses [abstract]. International Symposium on Neglected Influenza Viruses. Abstract No. O16.

Interpretive Summary:

Technical Abstract: Influenza A viruses (IAV) are endemic respiratory pathogens of swine that constitute a substantial economic burden to swine producers. Vaccination is the most commonly employed control measure, though the substantial diversity of IAV circulating in the US swine population adds tremendous challenges to effective vaccine formulation. The neuraminidase (NA) protein of IAV is a surface glycoprotein, important for the release of nascent virus particles from the cell surface. Though not as protective as neutralizing antibodies against the hemagglutinin (HA), antibodies against the NA can provide protection from influenza infection and transmission, particularly when HA immunity is diminished by drift. H3N2 and H1N2 viruses widely circulate in North American swine populations, but the N2 is divided into two distinct phylogenetic lineages resulting from introductions of human H3N2 in 1998 and 2002, with further genetic diversity within the 2 lineages. Here, we assessed the antigenic differences between and among 1998 and 2002 N2 lineages of swine IAV. N2 antigens were generated by reverse genetics on an irrelevant H9Nx backbone, with the N2 derived from viruses representing the contemporary phylogenetic diversity of N2-98 and N2-02 NA lineages. Using an enzyme-linked lectin assay (ELLA) we assessed neuraminidase inhibition (NI) titers using the H9Nx antigens and a panel of swine antisera against wild-type H3N2 or H1N2 viruses from four genetic clades within the N2-98 lineage; or the four genetic clades within the N2-02 lineage. Varying intra-lineage cross-reactivity was observed between N2-98 and N2-02 clades. Antisera raised against N2-98 antigens did not display cross-reactivity against N2-02 antigens, but antisera raised against N2-02 antigens had some cross-inhibitory activity against the limited panel of N2-98 antigens. Using antigenic cartography, we mapped the N2 antigens and calculated the antigenic distances between N2 lineages and clades. These preliminary results begin to identify the antigenic differences the two major N2 lineages circulating in North American swine populations and provide encouraging evidence for a need to expand the antigen and anti-sera panels within the predominant N2 phylogenetic clades. This will enable identification of specific residues contributing to antigenicity to improve vaccine strain selection and development.