Cross-protection between antigenically distinct H1N1 swine influenza viruses from Europe and North America
Article first published online: 17 AUG 2010
© 2010 Blackwell Publishing Ltd
Influenza and Other Respiratory Viruses
Volume 5, Issue 2, pages 115–122, March 2011
Total views since publication: 91
How to Cite
De Vleeschauwer, A. R., Van Poucke, S. G., Karasin, A. I., Olsen, C. W. and Van Reeth, K. (2011), Cross-protection between antigenically distinct H1N1 swine influenza viruses from Europe and North America. Influenza and Other Respiratory Viruses, 5: 115–122. doi: 10.1111/j.1750-2659.2010.00164.x
- Issue published online: 10 FEB 2011
- Article first published online: 17 AUG 2010
- Accepted 8 July 2010. Published Online 6 August 2010.
- H1N1 swine influenza virus;
- pandemic (H1N1) 2009;
- triple reassortant
Please cite this paper as: De Vleeschauwer et al. (2011) Cross-protection between antigenically distinct H1N1 swine influenza viruses from Europe and North America. Influenza and Other Respiratory Viruses 5(2), 115–122.
Background An avian-like H1N1 swine influenza virus (SIV) is enzootic in swine populations of Western Europe. The virus is antigenically distinct from H1N1 SIVs in North America that have a classical swine virus-lineage H1 hemagglutinin, as does the pandemic (H1N1) 2009 virus. However, the significance of this antigenic difference for cross-protection among pigs remains unknown.
Objectives We examined protection against infection with a North American triple reassortant H1N1 SIV [A/swine/Iowa/H04YS2/04 (sw/IA/04)] in pigs infected with a European avian-like SIV [A/swine/Belgium/1/98 (sw/B/98)] 4 weeks earlier. We also examined the genetic relationships and serologic cross-reactivity between both SIVs and with a pandemic (H1N1) 2009 virus [A/California/04/09 (Calif/09)].
Results After intranasal inoculation with sw/IA/04, all previously uninfected control pigs showed nasal virus excretion, high virus titers in the entire respiratory tract at 4 days post-challenge (DPCh) and macroscopic lung lesions. Most pigs previously infected with sw/B/98 tested negative for sw/IA/04 in nasal swabs and respiratory tissues, and none had lung lesions. At challenge, these pigs had low levels of cross-reactive virus neutralizing and neuraminidase inhibiting (NI) antibodies to sw/IA/04, but no hemagglutination-inhibiting antibodies. They showed similar antibody profiles when tested against Calif/09, but NI antibody titers were higher against Calif/09 than sw/IA/04, reflecting the higher genetic homology of the sw/B/98 neuraminidase with Calif/09.
Conclusions Our data indicate that immunity induced by infection with European avian-like H1N1 SIV affords protection for pigs against North American H1N1 SIVs with a classical H1, and they suggest cross-protection against the pandemic (H1N1) 2009 virus.