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. Webby
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.