Table of Contents
Influenza Research and Treatment
Volume 2012 (2012), Article ID 329029, 7 pages
Research Article

Comparison of Human-Like H1 ( 𝛿 -Cluster) Influenza A Viruses in the Swine Host

1Virus and Prion Diseases Research Unit, National Animal Disease Center, Agricultural Research Service, USDA, Ames, IA 50010, USA
2Labex-USA, Brazilian Agriculture Research Corporation (EMBRAPA), 70770-901 Brasília, DF, Brazil
3Embrapa Swine and Poultry Research Center, 89700-000 Concórdia, SC, Brazil
4College of Agronomy and Veterinary Medicine, University of Passo Fundo, 99052-900 Passo Fundo, RS, Brazil
5Department of Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, USA
6University of Minnesota Veterinary Diagnostic Laboratory, Saint Paul, MN 55108-1098, USA

Received 29 December 2011; Accepted 4 April 2012

Academic Editor: Ian Barr

Copyright © 2012 Janice R. Ciacci Zanella et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Influenza A viruses cause acute respiratory disease in swine. Viruses with H1 hemagglutinin genes from the human seasonal lineage ( 𝛿 -cluster) have been isolated from North American swine since 2003. The objective of this work was to study the pathogenesis and transmission of 𝛿 -cluster H1 influenza viruses in swine, comparing three isolates from different phylogenetic subclusters, geographic locations, and years of isolation. Two isolates from the 𝛿 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 𝛿 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.