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. 2013 Sep;87(17):9895-903.
doi: 10.1128/JVI.01038-13. Epub 2013 Jul 3.

Efficacy in pigs of inactivated and live attenuated influenza virus vaccines against infection and transmission of an emerging H3N2 similar to the 2011-2012 H3N2v

Crystal L Loving  1 , Kelly M Lager, Amy L Vincent, Susan L Brockmeier, Phillip C Gauger, Tavis K Anderson, Pravina Kitikoon, Daniel R Perez, Marcus E Kehrli Jr
Affiliations

Efficacy in pigs of inactivated and live attenuated influenza virus vaccines against infection and transmission of an emerging H3N2 similar to the 2011-2012 H3N2v

Crystal L Loving et al. J Virol. 2013 Sep.

Abstract

Vaccines provide a primary means to limit disease but may not be effective at blocking infection and pathogen transmission. The objective of the present study was to evaluate the efficacy of commercial inactivated swine influenza A virus (IAV) vaccines and experimental live attenuated influenza virus (LAIV) vaccines against infection with H3N2 virus and subsequent indirect transmission to naive pigs. The H3N2 virus evaluated was similar to the H3N2v detected in humans during 2011-2012, which was associated with swine contact at agricultural fairs. One commercial vaccine provided partial protection measured by reduced nasal shedding; however, indirect contacts became infected, indicating that the reduction in nasal shedding did not prevent aerosol transmission. One LAIV vaccine provided complete protection, and none of the indirect-contact pigs became infected. Clinical disease was not observed in any group, including nonvaccinated animals, a consistent observation in pigs infected with contemporary reassortant H3N2 swine viruses. Serum hemagglutination inhibition antibody titers against the challenge virus were not predictive of efficacy; titers following vaccination with a LAIV that provided sterilizing immunity were below the level considered protective, yet titers in a commercial vaccine group that was not protected were above that level. While vaccination with currently approved commercial inactivated products did not fully prevent transmission, certain vaccines may provide a benefit by limitating shedding, transmission, and zoonotic spillover of antigenically similar H3N2 viruses at agriculture fairs when administered appropriately and used in conjunction with additional control measures.

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Figures

Fig 1
Fig 1
Phylogeny of representative H3N2 influenza A virus isolates on the basis of the HA-encoding gene. The tree shown was constructed by the ML method and a GTR+Γ substitution model implemented in RAxML v.7.3.4. Values above or below branches indicate bootstrap support (percent) estimated from 1,000 resamplings of the sequence data; bootstrap values of ≤50% are not shown. H3N2 HA sublineages are indicated by the brackets on the right (clusters I, II, II, and IV). Taxon names indicate viral isolates, followed by GenBank or GISAID EpiFlu accession numbers in parentheses. LAIV vaccine isolates are marked with solid squares, and the challenge virus is marked with a solid diamond. The scale bar indicates the number of nucleotide substitutions per site.
Fig 2
Fig 2
Lung viral titers and pathology following primary challenge of vaccinated pigs. Groups of pigs were vaccinated with commercial killed swine IAV vaccine (KV) or experimental LAIV vaccine or sham vaccinated (NV) as described in Materials and Methods. Six weeks following primary immunization, pigs were intranasally challenged with rH3N2p virus and their lungs were collected at 5 dpi for evaluation of viral titers in BALF (A) and macroscopic (B) and microscopic (C) lung lesions. Each data point represents an individual animal in the vaccine group indicated.
Fig 3
Fig 3
Shedding dynamics following primary inoculation or natural acquisition of rH3N2p virus. Groups of pigs were vaccinated with commercial killed swine IAV vaccine (KV) or experimental LAIV vaccine or sham vaccinated (NV) as described in Materials and Methods. Six weeks following primary immunization, pigs in the principal group (A) were challenged intranasally with rH3N2p virus and NS was collected at 2, 4, and 5 dpi for quantification of viral titers. (B) At 2 dpi of principal pigs, naive pigs were placed in the same room as the principal pigs (indirect contact) in each respective vaccine group and NS was collected at the indicated time (dpc) for quantification of viral titers. Data are expressed as the mean + the standard error of the mean of each group. (C) Indirect correlation between the average viral titer in the NS of principal pigs (dpi 2, 4, and 5 averaged) and the day on which an NS from an indirect, naive contact was positive for virus.
Fig 4
Fig 4
Levels of antibodies specific to the rH3N2p challenge virus in the serum and nasal cavities of pigs following vaccination. Groups of pigs were vaccinated with commercial killed swine IAV vaccine (KV), experimental LAIV vaccine or sham vaccinated (NV) as described in Materials and Methods. Six weeks following primary immunization, samples were collected for evaluation of serum IgG (A) and NW IgA (B) levels. Data are expressed as the mean OD of each group ± the standard error of the mean.
Fig 5
Fig 5
Levels of antibodies specific to the rH3N2p challenge virus in BALF 5 days after a challenge. Groups of pigs were vaccinated with commercial killed swine IAV vaccine (KV) or experimental LAIV vaccine or sham vaccinated (NV), and 6 weeks following primary immunization, the pigs were challenged by the intranasal route with rH3N2p IAV. Five days following the challenge (Ch), BALF samples were collected and levels of IgG (A) and IgA (B) antibodies to the challenge virus were evaluated by ELISA as described in Materials in Methods. Data are expressed as the mean OD of each group ± the standard error of the mean.
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References

    1. Centers for Disease Control and Prevention (CDC) 2011. Swine-origin influenza A (H3N2) virus infection in two children—Indiana and Pennsylvania, July-August 2011. MMWR Morb. Mortal. Wkly. Rep. 60:1213–1215 - PubMed
    1. Brockwell-Staats C, Webster RG, Webby RJ. 2009. Diversity of influenza viruses in swine and the emergence of a novel human pandemic influenza A (H1N1). Influenza Other Respi. Viruses 3:207–213 - PMC - PubMed
    1. Ducatez MF, Hause B, Stigger-Rosser E, Darnell D, Corzo C, Juleen K, Simonson R, Brockwell-Staats C, Rubrum A, Wang D, Webb A, Crumpton JC, Lowe J, Gramer M, Webby RJ. 2011. Multiple reassortment between pandemic (H1N1) 2009 and endemic influenza viruses in pigs, United States. Emerg. Infect. Dis. 17:1624–1629 - PMC - PubMed
    1. Liu Q, Ma J, Liu H, Qi W, Anderson J, Henry SC, Hesse RA, Richt JA, Ma W. 2012. Emergence of novel reassortant H3N2 swine influenza viruses with the 2009 pandemic H1N1 genes in the United States. Arch. Virol. 157:555–562 - PubMed
    1. Richt JA, Lager KM, Janke BH, Woods RD, Webster RG, Webby RJ. 2003. Pathogenic and antigenic properties of phylogenetically distinct reassortant H3N2 swine influenza viruses cocirculating in the United States. J. Clin. Microbiol. 41:3198–3205 - PMC - PubMed

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