|GAUGER, PHILLIP - Iowa State University|
|GRAMER, MARIE - University Of Minnesota|
|DARNELL, DANIEL - St Jude Children’s Research Hospital|
|WEBBY, RICHARD - St Jude Children’s Research Hospital|
|SWENSON, SABRINA - Animal And Plant Health Inspection Service (APHIS)|
|KLIMOV, ALEXANDER - Centers For Disease Control And Prevention (CDCP) - United States|
Submitted to: Journal of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/23/2012
Publication Date: 6/1/2012
Citation: Kitikoon, P., Vincent, A.L., Gauger, P.C., Schlink, S.N., Bayles, D.O., Gramer, M.R., Darnell, D., Webby, R.J., Lager, K.M., Swenson, S.L., Klimov, A. 2012. Pathogenicity and transmission in pigs of the novel A(H3N2)v influenza virus isolated from humans and characterization of swine H3N2 viruses isolated in 2010-2011. Journal of Virology. 86(12):6804-6814.
Interpretive Summary: Influenza (flu) A viruses occasionally spread between pigs and humans. The best known example of this is the 2009 pandemic virus (pH1N1) that was generated from 2 different swine viruses, gained the ability to infect people, and then was spread by people to pigs around the world. Between July and December 2011, a new virus was detected in 12 humans in the United States. This virus contained genetic material from swine flu viruses as well as the pH1N1 and has been called A(H3N2)v by the World Health Organization. In this paper, we compared the properties of H3N2 viruses isolated from U.S. human and swine that inherited genes from typical swine flu viruses and the 2009 pH1N1 virus with different combinations to determine the ability of these viruses to spread in the swine population. Our results suggest that although certain combinations of gene segments may be required for the viruses to survive in pigs, all 3 viruses tested were able to infect and spread among pigs in our study. The A(H3N2)v from a human did not have any increased ability to infect, spread, or cause disease in pigs. It is essential to continue to monitor swine for flu viruses to understand how these viruses are changing and to detect when viruses are shared between pigs and people.
Technical Abstract: Swine influenza virus (SIV) H3N2 with triple reassorted internal genes (TRIG) has been enzootic in U.S. since 1998. Transmission of the 2009 pandemic H1N1 (pH1N1) virus to pigs in the U.S. was followed by reassortment with endemic SIV, resulting in reassorted viruses that include novel H3N2 genotypes (rH3N2p). Between July-December 2011, 12 cases of human infections with swine-lineage H3N2 viruses containing the pandemic matrix (pM) gene (A(H3N2)v) were detected. Whole genome analysis of H3N2 viruses isolated from pigs from 2009-2011 sequenced in this study and other available H3N2 sequence showed six different rH3N2p genotypes present in the U.S. swine population since 2009. The presence of the pM gene was a common feature among all rH3N2p genotypes, but no specific genotype appeared to predominate in the swine population. We compared the pathogenic, transmission, genetic, and antigenic properties of a human A(H3N2)v isolate and two swine H3N2 isolates, H3N2-TRIG and rH3N2p. Our in vivo study detected no increased virulence in A(H3N2)v or rH3N2p viruses compared to endemic H3N2-TRIG virus. Antibodies to cluster IV H3N2-TRIG and rH3N2p viruses had reduced cross-reactivity to A(H3N2)v compared to other cluster IV H3N2-TRIG and rH3N2p viruses. Genetic analysis of the hemagglutinin gene indicated that although rH3N2p and A(H3N2)v are related to cluster IV of H3N2-TRIG, some recent rH3N2p isolates appeared to be forming a separate cluster along with the human isolates of A(H3N2)v. Continued monitoring of these H3N2 viruses is necessary to evaluate evolution and potential loss of population immunity in swine and humans.