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Title: Pandemic H1N1 influenza: zoonoses are a two-way street

item Kehrli Jr, Marcus
item Baker, Amy
item Lager, Kelly
item Faaberg, Kay

Submitted to: United States Animal Health Association Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 11/16/2010
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Influenza is a zoonotic viral disease representing a worldwide health and economic threat to humans and animals. Swine influenza was first recognized clinically in pigs in the Midwestern United States in 1918 concurrent with the Spanish flu human pandemic. Since the first report that flu was caused by a virus in 1930, swine influenza virus (SIV) in pigs remained relatively stable up until the introduction in 1997/98 of novel human (HA, NA, PB1) and avian genes (PA, PB2) into viruses circulating in pigs. It has been demonstrated that these arose from 3 introductions of human H3N2, leading to phylogenetic clusters I, II, and III of SIV. All of the successful SIV reassortants that became endemic in the U.S. pig population characterized prior to 2009 contained a similar triple reassortant internal gene (TRIG) cassette including the PA and PB2 genes of avian lineage, NS, NP, and M genes of classical swine lineage, and the PB1 gene of human lineage. Since these human and avian genes were introduced into circulating SIVs, there appears to be an increase in genetic and antigenic diversity coincident with the acquisition of the TRIG cassette. Several additional introductions of influenza gene segments from human and avian viruses (H2N3) into circulating swine influenza viruses have been detected over the past decade. Since 2005, H1N1 and H1N2 viruses with the HA gene derived from human viruses have spread across the U.S. in swine herds forming the d-cluster H1 strains of SIV (there were at least two separate introductions of human seasonal HA from H1N2 and H1N1 viruses). Notably, in March-April 2009, a novel pandemic H1N1 emerged in the human population in North America. 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. The detection of novel viruses in both swine and humans led to a closer working relationship between the USDA and the Centers for Disease Control and Prevention in 2008. The interagency agreements put in place in 2008 were critical to the successful execution of the swine influenza research response conducted by ARS after the emergence of the 2009 A/H1N1 pandemic virus in humans. ARS was able to quickly obtain the virus from the CDC just days after its detection to develop differential diagnostic tests and demonstrate the pathogenesis of this virus in pigs, thus confirming the safety of pork. This research also enabled the rapid validation of a master seed virus for commercial swine 2009 A/H1N1 pandemic virus vaccines by the Center for Veterinary Biologics-USDA-APHIS. It is important to note that subsequent sequence analyses have shown that none of the 8 genes of the 2009 pandemic H1N1 cluster tightly with the genes of SIV circulating in the U.S. prior to the 2009 outbreak in humans, suggesting that neither the 2009 pandemic H1N1 nor closely related progenitor viral genes were present in U.S. swine influenza viruses prior to 2009. The 2009 pandemic H1N1, a virus shared between people and pigs, has the potential to further change the epidemiology of influenza viruses in human and swine populations. The 2009 pandemic H1N1 influenza was a highly visible demonstration that zoonoses are a two-way street. The One Health concept needs research and surveillance to be supported for both directions of the street in order for it