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Title:   Author  item
                                            Baker, Amyitem
                                            Lager, Kellyitem
                                            GAUGER, PHILLIP - Iowa State Universityitem
                                            GRAMER, MARIE - University Of Minnesotaitem
                                            CIACCI-ZANELLA, JANICE - Labex - Embrapa
  Submitted to: International Symposium on Emerging and Re-Emerging Pig Diseases
                                    Publication Type: Proceedings
                                    Publication Acceptance Date: 3/20/2011
                                    Publication  Date: 6/12/2011
                                    Citation: Vincent, A.L., Lorusso, A., Lager, K.M., Gauger, P.C., Gramer, M.R., Ciacci-Zanella, J.R. 2011. Influenza A virus in swine - moving beyond 2009. In: Proceedings of the 6th International Symposium on Emerging and Re-emerging Pig Diseases, June 12-15, 2011, Barcelona, Spain. p. 35-37.Interpretive Summary:
                                Technical Abstract: Introduction: Surveillance for influenza A viruses (IAV) circulating in pigs and other non-human mammals has been chronically underfunded and virtually nonexistent in many areas of the world [1]. This deficit is in spite of our knowledge that influenza is a disease shared between man and pig from at least as far back as the 1918 Spanish Flu Pandemic. In March-April 2009, a novel pandemic H1N1 emerged in the human population in North America [2] and demonstrated in a public forum the paucity of data on influenza viruses in swine. The gene constellation of the emerging virus was demonstrated to be a combination of genes from swine influenza A viruses (SIV) of North American and Eurasian lineages that had never before been identified in swine or other species. The emergent H1N1 quickly spread in the human population and the outbreak reached pandemic level 6 as declared by the World Health Organization on June 11, 2009. Although the 8 gene segments of the novel virus are similar to available sequences of corresponding genes from SIV from North America and Eurasia, no closely related ancestral IAV with this gene combination has been identified in North America or elsewhere in the world [3, 4]. Other than sporadic transmission to humans [5, 6], swine influenza A viruses of the H1N1 subtype historically have been distinct from avian and other mammalian H1N1 influenza viruses in characteristics of host specificity, serologic cross-reactivity, and/or nucleotide sequence. The emergence of the 2009 pandemic H1N1 (pH1N1) virus brought a heightened awareness to the evolution and epidemiology of influenza A viruses in swine and presents a new era of challenges and opportunities for understanding and controlling influenza in pigs.
  North American triple reassortant swine viruses. Swine influenza was first recognized in pigs in the Midwestern U.S. in 1918 as a respiratory disease that coincided with the human pandemic known as the Spanish flu. Since then, it has become an important disease to the swine industry throughout the world. The first influenza virus was isolated in 1930 by Shope [7] and was demonstrated to cause respiratory disease in swine that was similar to human influenza. The classical swine lineage H1N1 (cH1N1) derived from the 1918 pandemic was relatively stable at the genetic and antigenic levels in U.S. swine.
  The epidemiology of IAV in pigs dramatically changed after 1998 when triple reassortant viruses containing gene segments from the classical swine virus (NP, M, NS), human virus (PB1, HA, NA), and avian virus (PB2, PA) [8] became successfully established in the pig population [9]. The human lineage PB1, avian lineage PB2 and PA and swine lineage NP, M, and NS found in contemporary swine influenza viruses are referred to as the triple reassortant internal gene (TRIG) constellation [10] and the vast majority of the characterized swine viruses from the U.S. and Canada contain the TRIG, regardless of subtype.
  After their emergence, the H3N2 viruses reassorted with cH1N1 swine IAV [11, 12]. Reassortant H1 viruses are endemic with the H3N2 viruses in most major swine producing regions of the U.S. and Canada. Since 2005, H1N1 and H1N2 viruses with the HA gene derived from human viruses emerged and spread across the U.S. in swine herds [13]. The HAs from the human-like swine H1 viruses are genetically and antigenically distinct from classical swine lineage H1s. However, their TRIG genes are similar to those found in the TRIG cassette of the contemporary swine triple reassortant viruses.
  To represent the evolution of the currently circulating North American H1 viruses, a cluster classification has been proposed. Viruses from the classical H1N1 lineage-HA evolved to form alpha-, beta-, and gamma-clusters based on the genetic makeup of the HA gene; whereas H1 subtypes strains with HA genes most similar to human seasonal H1 vi


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