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Title:   Author  item
                                            GAUGER, PHILLIP - Iowa State Universityitem
                                            Baker, Amy
  Submitted to: Swine Disease Conference Proceedings
                                    Publication Type: Proceedings
                                    Publication Acceptance Date: 11/10/2011
                                    Publication  Date: 11/10/2012
                                    Citation: Gauger, P.C., Vincent, A.L. 2012. Swine influenza virus: epidemiology and vaccine concerns. In: Proceedings of the 19th Annual Swine Disease Conference for Swine Practitioners, November 10-11, 2011, Ames, Iowa. p. 13-21.Interpretive Summary:
                                Technical Abstract: Introduction. Swine influenza virus (SIV) is a primary cause of respiratory disease in swine and a component of the porcine respiratory disease complex (PRDC). Influenza viruses are an important health and economic concern for swine producers throughout the world. Swine operations may be affected by seasonal infections or endemic circulation of SIV's resulting in high morbidity but typically low mortality. Infection with SIV manifests as an acute onset of respiratory disease characterized by fever, lethargy, anorexia, respiratory distress, coughing, conjunctivitis and nasal discharge (Alexander and Brown, 2000; McQueen et al., 1968; Olson et al., 1999; Richt et al., 2003). Reproductive failure associated with SIV-induced fever has also been documented, which may include infertility, abortions and weak-born piglets (Karasin et al., 2000; Wallace and Elm, Jr., 1979; Wesley, 2004). Influenza is a zoonotic viral disease that represents a health and economic threat to both humans and animals worldwide.
 The epidemiology of influenza viruses in swine has become more complicated after the introduction of the human-swine-avian lineage triple reassortant influenza virus in 1998. The rate of genetic change within the different subtypes has dramatically increased, antigenic variants of the virus are emerging at a rapid pace, the disease does not consistently follow a predictable seasonal pattern as in the past and vaccines often lack adequate cross-protection against these emerging diverse strains. In addition, the genetic similarity between swine and human influenza viruses and the ease of transmission between these populations suggests a change in the terminology away from "swine influenza virus" to the more generic "influenza A viruses" (IAV) in swine is appropriate.
 The complex ecology and epidemiology characteristic of contemporary IAV's may be attributed to unique characteristics and interactions between the virus, the host (swine) and three events that have had an impact on the evolution of IAV's in swine. These include the introduction of the triple reassortant viruses in North American swine in 1998, introduction of human seasonal H1 viruses in North American swine in 2005 and the 2009 swine-origin H1N1 influenza pandemic.
 The Virus. Influenza A viruses in swine are members of the Orthomyxoviridae family with segmented, single-stranded, negative-sense RNA genomes (Knipe et al., 2007). The surface glycoproteins hemagglutinin (HA) and neuraminidase (NA) are important to the pathogenesis and life cycle of influenza viruses and are the targets of the host humoral immune response (Cox et al., 2004). Only the H1, H3, N1 and N2 subtypes are endemic and currently circulate in North American swine. The HA and NA genes may vary due to two types of processes known as antigenic drift and antigenic shift. Drift results in minor changes in the genome due to polymerase errors during replication and occurs more commonly in RNA viruses in general. Antigenic shift occur when two or more viruses infect the same cell and exchange entire HA or NA gene segments resulting in a reassortant virus. Prior human influenza pandemics were the result of antigenic shift or a complete species jump of avian IAV to humans (Kawaoka et al., 1989).
 The Host. Swine are a natural host for influenza viruses. The HA protein is responsible for viral attachment and entry into the host respiratory epithelial cell where the virus replicates. Lesions induced by influenza virus infection include a necrotizing bronchiolitis and interstitial pneumonia. The HA plays a critical role in the restriction of interspecies transmission of influenza viruses based on the specific binding capacity of the HA protein and it's affinity for the host cell receptor. Influenza viruses bind to sialic acid receptors located on the surface of respiratory epithelial cells. However, mammalian and av


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