|Ciacci Zanella, Janice|
Submitted to: Influenza Research and Treatment
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/4/2012
Publication Date: 6/4/2012
Citation: Ciacci Zanella, J.R., Vincent, A.L., Zanella, E.L., Lorusso, A., Loving, C.L., Brockmeier, S.L., Gauger, P.C., Janke, B.H., Gramer, M.R. 2012. Comparison of human-like H1 (delta-cluster) influenza A viruses in the swine host. Influenza Research and Treatment. Available: http://www.hindawi.com/journals/irt/2012/329029/. Interpretive Summary: Influenza A viruses cause acute respiratory disease in swine and are common in many swine herds. Influenza infections in swine are typically caused by swine specific strains that commonly circulate in given geographic regions, but occasionally new strains emerge and become established in the pig population. Influenza viruses with surface proteins found on the human seasonal H1N1 and H1N2 viruses from 2003-2005 were recently found to infect pigs and to have mixed with the common swine viruses. These human-like viruses have since become established in the United States pig population. The objective of this work was to study these human-like influenza viruses in a pig infection and transmission model, comparing three isolates from different geographic locations and years. All isolates caused respiratory disease and spread from pig to pig. However, differences between the viruses were observed and these differences may have implications for detection, vaccine development, and disease control strategies for pigs.
Technical Abstract: Influenza A viruses cause acute respiratory disease in swine. Viruses with H1 hemagglutinin genes from the human seasonal lineage (delat cluster) have been isolated from North American swine since 2003. The objective of this work was to study the pathogenesis and transmission of delta cluster H1 influenza viruses in swine, comparing three isolates from different phylogenetic sub-clusters, geographic locations, and years of isolation. Two isolates from the delta2 sub-cluster, 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 delta1 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 post infection MN07 infected pigs had lower virus titers in the nose and lung 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.