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Title: Swine Influenza Virus: Emerging Understandings

item Baker, Amy
item Lager, Kelly
item GAUGER, PHILLIP - Iowa State University
item GRAMER, MARIE - University Of Minnesota
item CIACCI-ZANELLA, JANICE - Labex - Embrapa

Submitted to: Swine Disease Conference Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 10/2/2010
Publication Date: 11/4/2010
Citation: Vincent, A.L., Lorusso, A., Lager, K.M., Gauger, P.C., Gramer, M.R., Ciacci-Zanella, J.R. 2010. Swine influenza virus: emerging understandings. In: Proceedings of 18th Annual Swine Disease Conference for Swine Practitioners, November 4-5, 2010, Ames, IA. p. 57-62.

Interpretive Summary:

Technical Abstract: Introduction: In March-April 2009, a novel pandemic H1N1 emerged in the human population in North America [1]. 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 SIV with this gene combination has been identified in North America or elsewhere in the world [2-3]. Other than sporadic transmission to humans [4-5], 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 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. The hemagglutinin (HA) and the neuraminidase (NA) proteins encoded by gene segments 4 and 6, respectively, play a key role in the influenza life cycle and represent the primary targets of the host humoral immune response [6]. Both HA and NA undergo two types of variation called antigenic drift and antigenic shift. Antigenic drift involves minor changes in the HA and NA genes due to polymerase errors during replication, whereas antigenic shift involves major changes in these molecules resulting from replacement of the entire gene segment as a consequence of reassortment in the event that two (or more) unique viruses infect the same cell. Based upon the HA and NA proteins, 16 HA and 9 NA subtypes, naturally paired in different combinations, have been identified thus far [7]. Only a limited number of subtypes have been established in mammals. Only viruses of H1, H2, H3, N1 and N2 [8] subtypes have circulated widely in the human population and only H1, H3, N1 and N2 subtypes have been consistently isolated from pigs [9]. 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 [10] and was demonstrated to cause respiratory disease in swine that was similar to human influenza. This strain was subsequently recognized belonging to the H1N1 lineage of influenza virus, and swine were utilized in the following years as a model to study influenza pathogenesis in a natural host. From the first characterization of swine influenza virus until the late 1990s, the classical swine lineage H1N1 (cH1N1) was relatively stable at the genetic and antigenic levels in U.S. swine. North American triple reassortant swine viruses: The epidemiology of influenza in pigs dramatically changed after 1997-1998. In 1998, a severe influenza-like disease was observed in pigs in North Carolina with additional outbreaks in swine herds in Minnesota, Iowa, and Texas. The causative agents for these outbreaks were identified as influenza A viruses of the H3N2 subtype. Genetic analysis of these H3N2 viruses demonstrated the presence of two different genotypes. However, only triple reassortants containing gene segments from the classical swine virus (NP, M, NS), human virus (PB1, HA, NA). and avian virus (PB2, PA) [11] became successfully established in the pig population. By the end of 1999, viruses antigenically and genetically r