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Title:   Author  item
                                            Kitikoon, Pravinaitem
                                            Baker, Amyitem
                                            GAUGER, PHILLIP - Iowa State Universityitem
                                            Schlink, Sarahitem
                                            Bayles, Darrellitem
                                            GRAMER, MARIE - University Of Minnesotaitem
                                            DARNELL, DANIEL - St Jude Children’s Research Hospitalitem
                                            WEBBY, RICHARD - St Jude Children’s Research Hospitalitem
                                            Lager, Kellyitem
                                            SWENSON, SABRINA - Animal And Plant Health Inspection Service (APHIS)item
                                            KLIMOV, ALEXANDER - Centers For Disease Control And Prevention (CDC) - United States
  Submitted to: American Society for Virology Meeting
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 5/1/2012
                                    Publication  Date: 7/21/2012
                                    Citation: Kitikoon, P., Vincent, A.L., Gauger, P., Schlink, S.N., Bayles, D.O., Gramer, M., Darnell, D., Webby, R., Lager, K.M., Swenson, S., Klimov, A. 2012. Comparison of 2010-2011 H3N2 influenza A viruses isolated from swine and the A(H3N2)v isolated from humans in 2011 [abstract]. American Society for Virology 31st Annual Meeting. p. 102.Interpretive Summary:
                                Technical Abstract: In the end of 2011, 12 U.S. cases of humans infected with swine H3N2 virus containing the matrix gene from pandemic H1N1 2009 virus (H1N1pdm09) were detected and named A(H3N2)v. This study used a swine model to compare the pathogenic, transmission, genetic, and antigenic properties of a human A(H3N2)v isolate and two swine H3N2 isolates, H3N2-TRIG (endemic in U.S. swine) and rH3N2p (novel reassorted H1N1pdm09/H3N2-TRIG genotypes). Fifty-six pigs were divided into four groups of eight including: negative controls; A(H3N2)v-infected; H3N2-TRIG-infected and rH3N2p-infected pigs. Eight contact pigs were comingled with each of the infected groups to study virus transmission. Whole genome analysis showed six different rH3N2p genotypes present in the U.S. swine population since 2009. The pM was a common feature among all rH3N2p genotypes. The H1N1pdm09/H3N2-TRIG reassortment likely occurred as multiple events. No specific rH3N2p genotype appeared to predominate in the swine population during the time period sampled. HA gene analysis indicated that rH3N2p and A(H3N2)v are related to the contemporary H3N2-TRIG virus but a number of recent rH3N2p swine isolates formed a separate cluster with the human isolates of A(H3N2)v. Our in vivo study demonstrated no enhanced phenotype in the A(H3N2)v- or rH3N2p-infected pigs. Antibodies to H3N2-TRIG virus cross-reacted to both reassortant H3N2 viruses; however, the A(H3N2)v virus had reduced cross-reactivity to the other H3N2 antisera tested. Continued monitoring of this group of H3N2 viruses through whole genome analysis and antigenic cross-reactivity is necessary to evaluate population immunity in both swine and humans. As influenza A viruses continue to evolve and are readily shared between humans and animals, the role of pigs in generating reassortant influenza viruses cannot be overlooked. Additionally, in vivo studies in swine are essential to examine the phenotypic nature of these novel emerging viruses in their natural host.


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