Influenza A viruses cause acute respiratory disease in swine. Viruses with H1 hemagglutinin genes from the human seasonal lineage ( -cluster) have been isolated from North American swine since 2003. The objective of this work was to study the pathogenesis and transmission of -cluster H1 influenza viruses in swine, comparing three isolates from different phylogenetic subclusters, geographic locations, and years of isolation. Two isolates from the 2 subcluster, A/sw/MN/07002083/07 H1N1 (MN07) and A/sw/IL/00685/05 H1N1 (IL05), and A/sw/TX/01976/08 H1N2 (TX08) from the 1 sub-cluster were evaluated. All isolates caused disease and were transmitted to contact pigs. Respiratory disease was apparent in pigs infected with MN07 and IL05 viruses; however, clinical signs and lung lesions were reduced in severity as compared to TX08. On day 5 following infection MN07-infected pigs had lower virus titers than the TX08 pigs, suggesting that although this H1N1 was successfully transmitted, it may not replicate as efficiently in the upper or lower respiratory tract. MN07 and IL05 H1N1 induced higher serum antibody titers than TX08. Greater serological cross-reactivity was observed for viruses from the same HA phylogenetic sub-cluster; however, antigenic differences between the sub-clusters may have implications for disease control strategies for pigs. 1. Introduction Influenza A viruses are important infectious agents for humans, avian species, and many mammalian species, including swine. In swine, influenza virus causes an acute infection characterized by high morbidity and very low mortality rates [1]. Influenza viruses of the family Orthomyxoviridae have negative-sense single-stranded eight-segmented genome encoding for up to twelve structural and accessory proteins [2]. The triple reassortant internal gene constellation (TRIG) is the common backbone of the swine influenza viruses currently circulating in North America (for a review, see Vincent et al., 2008 [3]). Within the TRIG viruses, a dominant circulating genotype carries the HA and NA encoding genes of the human seasonal viruses of the H1 lineage (hu-like), identified from pigs in American and Canadian herds [4]. The HA genes of these viruses form the δ-cluster in phylogenetic analyses of HA genes from North American influenza A viruses of swine. Contemporary δ-cluster HA genes can be further divided into two sub-clusters, δ1 and δ2 [5]. Phylogenetically, the HA sequences of American and Canadian δ-cluster influenza A viruses appeared to have been derived from at least two independent human-to-pig transmission
References
[1]
C. W. Olsen, “The emergence of novel swine influenza viruses in North America,” Virus Research, vol. 85, no. 2, pp. 199–210, 2002.
[2]
R. A. Lamb and R. M. Krug, “Orthomyxoviridae: the viruses and their replication,” in Fields Virology, D. M. Knipe, P. M. Howley, D. E. Griffin, et al., Eds., pp. 1487–1531, Lippincott Williams & Wilkins, Philadelphia, Pa, USA, 2007.
[3]
A. L. Vincent, W. Ma, K. M. Lager, B. H. Janke, and J. A. Richt, “Swine influenza viruses. A North American perspective,” Advances in Virus Research, vol. 72, pp. 127–154, 2008.
[4]
A. I. Karasin, S. Carman, and C. W. Olsen, “Identification of human H1N2 and human-swine reassortant H1N2 and H1N1 influenza A viruses among pigs in Ontario, Canada (2003 to 2005),” Journal of Clinical Microbiology, vol. 44, no. 3, pp. 1123–1126, 2006.
[5]
A. Lorusso, A. L. Vincent, M. L. Harland et al., “Genetic and antigenic characterization of H1 influenza viruses from United States swine from 2008,” Journal of General Virology, vol. 92, no. 4, pp. 919–930, 2011.
[6]
A. L. Vincent, W. Ma, K. M. Lager, M. R. Gramer, J. A. Richt, and B. H. Janke, “Characterization of a newly emerged genetic cluster of H1N1 and H1N2 swine influenza virus in the United States,” Virus Genes, vol. 39, no. 2, pp. 176–185, 2009.
[7]
J. Prickett, R. Simer, J. Christopher-Hennings, K. J. Yoon, R. B. Evans, and J. J. Zimmerman, “Detection of Porcine reproductive and respiratory syndrome virus infection in porcine oral fluid samples: a longitudinal study under experimental conditions,” Journal of Veterinary Diagnostic Investigation, vol. 20, no. 2, pp. 156–163, 2008.
[8]
P. G. Halbur, P. S. Paul, M. L. Frey et al., “Comparison of the pathogenicity of two US porcine reproductive and respiratory syndrome virus isolates with that of the Lelystad virus,” Veterinary Pathology, vol. 32, no. 6, pp. 648–660, 1995.
[9]
J. A. Richt, K. M. Lager, B. H. Janke, R. D. Woods, R. G. Webster, and R. J. Webby, “Pathogenic and antigenic properties of phylogenetically distinct reassortant H3N2 swine influenza viruses cocirculating in the United States,” Journal of Clinical Microbiology, vol. 41, no. 7, pp. 3198–3205, 2003.
[10]
E. Spackman and D. L. Suarez, “Type a influenza virus detection and quantitation by real-time RT-PCR,” Methods in Molecular Biology, vol. 436, pp. 19–26, 2008.
[11]
P. Kitikoon, D. Nilubol, B. J. Erickson et al., “The immune response and maternal antibody interference to a heterologous H1N1 swine influenza virus infection following vaccination,” Veterinary Immunology and Immunopathology, vol. 112, no. 3-4, pp. 117–128, 2006.
[12]
L. J. Reed and H. Muench, “A simple method of estimating fifty per cent endpoints,” American Journal of Epidemiology, vol. 27, no. 3, pp. 493–497, 1938.
[13]
A. L. Vincent, S. L. Swenson, K. M. Lager, P. C. Gauger, C. Loiacono, and Y. Zhang, “Characterization of an influenza A virus isolated from pigs during an outbreak of respiratory disease in swine and people during a county fair in the United States,” Veterinary Microbiology, vol. 137, no. 1-2, pp. 51–59, 2009.
[14]
M. I. Nelson, P. Lemey, Y. Tan et al., “a virus in north american swine,” PLoS Pathogens, vol. 7, no. 6, Article ID e1002077, 2011.
[15]
H. Liu, J. Xing, J. Pan, Q. Yang, and Y. Zhao, “Construction and immunogenicity analysis of antigenic epitopes of Swine influenza virus,” Shengwu Gongcheng Xuebao, vol. 24, no. 4, pp. 690–694, 2008.
[16]
L. M. Chen, P. Rivailler, J. Hossain et al., “Receptor specificity of subtype H1 influenza A viruses isolated from swine and humans in the United States,” Virology, vol. 412, no. 2, pp. 401–410, 2011.
[17]
S. G. M. Van Poucke, J. M. Nicholls, H. J. Nauwynck, and K. Van Reeth, “Replication of avian, human and swine influenza viruses in porcine respiratory explants and association with sialic acid distribution,” Virology Journal, vol. 7, article 38, 2010.
[18]
T. Ito, J. N. S. S. Couceiro, S. Kelm et al., “Molecular basis for the generation in pigs of influenza A viruses with pandemic potential,” Journal of Virology, vol. 72, no. 9, pp. 7367–7373, 1998.
