Influenza A Virus Diversity and Transmission in Exhibition Swine

Swine are permissive to infections with both avian and human influenza Aviruses, facilitating genomic reassortment among viruses from multiple host species. As a result, swine have been identified as mixing vessels for influenza A viruses and a source of emergence for novel viruses, including those with pandemic potential [1, 2]. Since July 2011, human infections with influenza A virus of swine (IAV-S) subtype H3N2 (H3N2v to distinguish them from seasonal H3N2 influenza A viruses) have occurred throughout the United States with more than 340 cases and 1 death (as of July 2015) [3]. The main risk factor for infection with H3N2v was identified as direct contact with swine, primarily during agricultural fairs [4]. There are 3 major swine-human interfaces in the United States: domestic swine (commercial swine and exhibition swine), feral hogs (hunted for sport, food, and animal control), and abattoirs. It is estimated that some 150 million people visit agricultural fairs in North America annually, allowing for considerable contact with live swine [5]. This is more than for any other interface in the United States. Furthermore, agricultural fairs allow for prolonged commingling of pigs from numerous breeders andmultiple states. Collectively, these contacts create an environment conducive to zoonotic transmission, potential for viral reassortment with other strains, and geographic spread of influenza Aviruses to new regions. Yet, surveillance, risk assessment, and evolutionary studies of IAV-S at the domestic swine-human interface have been conducted mainly in commercial swine [6–10], and little is known about the diversity of influenza A viruses circulating in exhibition swine. While control measures addressing activities before, during, and after swine exhibitions [11] reduced the infection risk (as demonstrated by the absence of human cases to date in 2015), H3N2v continues to circulate among North American swine and, as such, has high pandemic potential. In this issue of The Journal of Infectious Disease, Nelson and colleagues [12] present results from the largest molecular epidemiology study of influenza A viruses in exhibition swine to date. They carried out large-scale comparative genomic and statistical phylogenetic analyses to provide a detailed picture of the evolution and spread of the IAV-S in exhibition swine in the United States during 2009–2013. They showed annual introductions of IAV-S to exhibition swine from commercial pigs. Yet, similar genotypes circulate in exhibition swine in neighboring states, suggesting that viral transmission and genetic exchange among viruses are found exclusively in exhibition swine populations. Movement of exhibition swine, therefore, may create opportunities for IAV-S to transmit to naive populations and generate novel influenza variants through reassortment. Even though there is evidence of direct transmission of human IAV to exhibition swine, this occurred less often than swine-to-human transmission. The manners in which these H3N2v viruses have become established in exhibition swine suggest that exhibition swine should be considered a unique reservoir for influenza viruses with pandemic potential. This study provides a framework to generate testable hypotheses and insights into specific risk assessments for potentially pandemic influenza strains. Even though the viruses in exhibition swine are ultimately derived from those circulating in commercial herds, the conditions at agricultural fairs, and the rearing behaviors of exhibition swine, allow those viruses to diversify from their common ancestors. Control efforts, such as prepandemic vaccine stockpiling, designed to target viruses circulating in commercial swine might not be effective against viruses circulating in exhibitions swine. The fact that many more people have direct contact with exhibition swine than commercial swine means that risk mitigation must also account for the diversity of viruses circulating among exhibition swine. Therefore, large-scale comparative genetic Received and accepted 24 July 2015; published online 4 August 2015. Correspondence: J. Bahl, Center for Infectious Diseases, School of Public Health, The University of Texas Health Science Center at Houston, 1200 Pressler St, Houston, TX 77030 ([email protected]). The Journal of Infectious Diseases 2016;213:169–70 © The Author 2015. Published by Oxford University Press for the Infectious Diseases Society of America. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http:// creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, contact [email protected]. DOI: 10.1093/infdis/jiv400