Volume 17, Number 9–September 2011
Research
Multiple Reassortment between Pandemic (H1N1) 2009 and Endemic Influenza Viruses in Pigs, United States
Mariette F. Ducatez, Ben Hause, Evelyn Stigger-Rosser, Daniel Darnell, Cesar Corzo, Kevin Juleen, Randy Simonson, Christy Brockwell-Staats, Adam Rubrum, David Wang, Ashley Webb, Jeri-Carol Crumpton, James Lowe, Marie Gramer, and Richard J. WebbyAuthor affiliations: St. Jude Children's Research Hospital, Memphis, Tennessee, USA (M.F. Ducatez, E. Stigger-Rosser, D. Darnell, C. Brockwell-Staats, A. Rubrum, D. Wang, A. Webb, J.-C. Crumpton, R.J. Webby); Newport Laboratories, Worthington, Minnesota, USA (B. Hause, R. Simonson); University of Minnesota College of Veterinary Medicine, Saint Paul, Minnesota, USA (C. Corzo, K. Juleen, M. Gramer); and Carthage Veterinary Services, Carthage, Illinois, USA (J. Lowe)
Suggested citation for this article
Abstract
As a result of human-to-pig transmission, pandemic influenza A (H1N1) 2009 virus was detected in pigs soon after it emerged in humans. In the United States, this transmission was quickly followed by multiple reassortment between the pandemic virus and endemic swine viruses. Nine reassortant viruses representing 7 genotypes were detected in commercial pig farms in the United States. Field observations suggested that the newly described reassortant viruses did not differ substantially from pandemic (H1N1) 2009 or endemic strains in their ability to cause disease. Comparable growth properties of reassortant and endemic viruses in vitro supported these observations; similarly, a representative reassortant virus replicated in ferrets to the same extent as did pandemic (H1N1) 2009 and endemic swine virus. These novel reassortant viruses highlight the increasing complexity of influenza viruses within pig populations and the frequency at which viral diversification occurs in this ecologically important viral reservoir.
Since its detection in humans in April 2009 (1), the pandemic influenza A (H1N1) 2009 virus spread quickly throughout the world. The pandemic virus was first detected in pigs in Canada in early May 2009 (2), and at least 14 countries have reported pigs infected with pandemic (H1N1) 2009 viruses (3), a few of which have been thoroughly described in the literature: in the Americas during summer 2009 (4,5); in Norway and Italy during fall 2009 (6,7); in India in May, June, and November 2009 (8); in Hong Kong Special Administrative Region, People's Republic of China, during October 2009–January 2010 (9); and in South Korea and Thailand during December 2009 (10,11). All of these infections were caused by human-to-pig transmission.As a result of human-to-pig transmission, pandemic influenza A (H1N1) 2009 virus was detected in pigs soon after it emerged in humans. In the United States, this transmission was quickly followed by multiple reassortment between the pandemic virus and endemic swine viruses. Nine reassortant viruses representing 7 genotypes were detected in commercial pig farms in the United States. Field observations suggested that the newly described reassortant viruses did not differ substantially from pandemic (H1N1) 2009 or endemic strains in their ability to cause disease. Comparable growth properties of reassortant and endemic viruses in vitro supported these observations; similarly, a representative reassortant virus replicated in ferrets to the same extent as did pandemic (H1N1) 2009 and endemic swine virus. These novel reassortant viruses highlight the increasing complexity of influenza viruses within pig populations and the frequency at which viral diversification occurs in this ecologically important viral reservoir.
In the United States, H1N1 subtypes of the classical swine influenza lineage (now designated as H1α) dominated from 1918 through 1998. In ≈1998, influenza (H3N2) triple reassortant viruses appeared, accompanied by a transient increase in disease severity (12,13). These triple reassortants contained polymerase acidic (PA) and polymerase basic 2 (PB2) genes of avian virus origin; hemagglutinin (HA), neuraminidase (NA), and polymerase basic 1 (PB1) genes of human virus origin; and matrix (M), nucleoprotein (NP) and nonstructural (NS) genes of classical swine virus origin (13). After these viruses appeared, multiple reassortment occurred that combined different HA and NA genes with the triple reassortant internal gene (TRIG) cassette (PA, PB1, PB2, NP, M, and NS) (14–20).
In addition to H1α, 3 distinct lineages of H1 hemagglutinin have been defined and characterized: H1β strains, first detected in 2001–2002; H1δ (or "seasonal human-like" swine H1) strains in 2003–2005; and H1γ strains in 1999–2000 (19,21). Soon after the appearance of pandemic (H1N1) 2009 viruses (whose HA clusters with the swine H1γ viruses) in pigs, the first reassortment event with an endemic swine influenza virus was reported in pigs in Hong Kong. This virus, A/swine/201/2010, contained a Eurasian swine lineage HA, a pandemic (H1N1) 2009 NA, with the TRIG cassette (9). Subsequently, a reassortant with 7 pandemic (H1N1) 2009 gene segments and a swine N2 gene was found in Italy (22), and a reassortant with 7 pandemic (H1N1) 2009 gene segments and a swine N1 gene was found in Germany (23). Considering the known circulation of TRIG-containing endemic and pandemic (H1N1) 2009 viruses in pigs, the chance for similar reassortment to occur in the United States also seemed high.
We describe the isolation of 9 pandemic (H1N1) 2009/endemic swine reassortant influenza viruses representing 7 distinct genotypes in pigs in the United States. Our study highlights the effect of reverse zoonotic transmission of the pandemic virus on this population.
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Reassortment between Influenza Viruses in Pigs | CDC EID: - Enviado mediante la barra Google
Suggested Citation for this Article
Ducatez MF, Hause B, Stigger-Rosser E, Darnell D, Corzo C, Juleen K, et al. Multiple reassortment between pandemic (H1N1) 2009 and endemic influenza. Emerg Infect Dis [serial on the Internet]. 2011 Sep [date cited]. http://dx.DOI.org/10.3201/1709.110338DOI: http://dx.DOI.org/10.3201/1709.110338
Comments to the Authors
Please use the form below to submit correspondence to the authors or contact them at the following address:
Richard J. Webby, Department of Infectious Diseases, St. Jude Children's Research Hospital, 262 Danny Thomas Pl, Memphis, TN 38105-3678, USA; email: richard.webby@stjude.org
Richard J. Webby, Department of Infectious Diseases, St. Jude Children's Research Hospital, 262 Danny Thomas Pl, Memphis, TN 38105-3678, USA; email: richard.webby@stjude.org
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