Author
Loving, Crystal | |
Baker, Amy | |
Brockmeier, Susan | |
GAUGER, PHILLIP - Iowa State University | |
PEREZ, DANIEL - University Of Maryland | |
KHURANA, SURENDE - Food And Drug Administration(FDA) | |
GOLDING, HANA - Food And Drug Administration(FDA) |
Submitted to: Gordon Research Conference Proceedings
Publication Type: Abstract Only Publication Acceptance Date: 10/13/2011 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Endemic strains of influenza A virus (IAV) in North America pigs consist of the subtypes H1N1, H1N2, and H3N2. These circulating strains contain the triple reassortant internal gene (TRIG) cassette resulting from incorporation of genes from swine, avian, and human IAV's. Genetic drift and reassortment have resulted in four H1 phylogenetic clusters and all currently co-circulate in US swine. Inactivated IAV vaccines do not provide adequate protection to heterologous homosubtypic IAV, nor heterosubtypic IAV and may even lead to vaccine associated enhanced respiratory disease (VAERD). In pigs, vaccination with an inactivated H1N2 IAV (MN08) resulted in enhanced disease following challenge with pandemic H1N1 IAV (CA09). Levels of proinflammatory cytokines IL-8, IL-1 and IL-6 in the lungs were significantly increased in the VAERD group, whereas the antiviral cytokine IFNa was significantly decreased in the VAERD group. There was no detectable antibody to the HA1 region of CA09 following vaccination with inactivated MN08, though there was cross-reactive antibody to the HA2 region that could increase infectivity of CA09. Interestingly, this enhancement does not occur following vaccination with a modified-live MN08 IAV. IAV in pigs predisposes to secondary bacterial infection with Haemophilus, regardless of VAERD. With the continued emergence of unique antigenic subtypes the need for an effective IAV vaccine in pigs remains high, and control of bacterial infection and spreading is critical when IAV outbreaks occur. |