Global coordination for swine influenza virus surveillance and research: what are we missing from the big picture?

Authors: Baker, Amy; Kitikoon, Pravina; GAUGER, P - Iowa State University; GRAMER, M - University Of Minnesota; Lorusso, Alessio; Lager, Kelly; CIACCI-ZANELLA, J - Labex - Embrapa

Submitted to: American Association of Swine Veterinarians Annual Meeting
Publication Type: Proceedings
Publication Acceptance Date: 11/30/2011
Publication Date: 3/10/2012
Citation: Vincent, A.L., Kitikoon, P., Gauger, P.C., Gramer, M.R., Lorusso, A., Lager, K.M., Ciacci-Zanella, J.R. 2012. Global coordination for swine influenza virus surveillance and research: what are we missing from the big picture? In: Proceedings of the 43rd American Association of Swine Veterinarians Annual Meeting, March 10-13, 2012, Denver, Colorado. p. 507-512.

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. This deficit continues 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 and demonstrated in a very public forum the paucity of data on influenza viruses in swine. This scrutiny continues. 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 had been identified in North America or elsewhere in the world. Other than sporadic transmission to humans, 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. Unfortunately, these opportunities have yet to be significantly realized in a better understanding of the ecology and evolution of IAV in swine, despite the passage of 2 years and investment of resources. North American triple reassortant 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, influenza has become an important disease to the swine industry throughout the world. The first influenza virus was isolated in 1930 by Shope 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 for nearly 80 years. 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) became successfully established in the pig population. 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. After their emergence, the H3N2 viruses reassorted with cH1N1 swine IAV. Reassortant H1 viruses are endemic with the H3N2 viruses in most major swine producing regions of the U.S. and Canada and since early in the new millennium, the vast majority of the fully characterized swine viruses contain the TRIG, regardless of subtype. Outside of North America, genetically related swine viruses that contain the TRIG have been identified in Korea, Vietnam, and China. Important to note, North American TRIG-containing swine viruses readily infect turkeys, which may play an unappreciated role in the epidemiology of SIV. Since 2005, H1N1 and H1N2 viruses with the HA gene derived from human seasonal IAV emerged and spread across the U.S. in swine herds. The HAs from the human-like swine H1 viruses are genetically and antigenica