Pandemic (H1N1) 2009 influenza A virus was detected in Norwegian pigs in October 2009. Until then, Norway was regarded free of swine influenza. Intensified screening revealed 91 positive herds within three months. The virus was rapidly transmitted to the susceptible population, including closed breeding herds with high biosecurity. Humans were important for the introduction as well as spread of the virus to pigs. Mild or no clinical signs were observed in infected pigs. Surveillance of SIV in 2010 revealed that 41% of all the Norwegian pig herds had antibodies to pandemic (H1N1) 2009 virus. Furthermore, this surveillance indicated that pigs born in positive herds after the active phase did not seroconvert, suggesting no ongoing infection in the herds. However, results from surveillance in 2011 show a continuing spread of the infection in many herds, either caused by new introduction or by virus circulation since 2009. 1. Introduction Swine influenza A viruses (SIVs) are enzootic in most European pig populations [1]. The SIV H1N1 and H3N2 subtypes have been circulating for more than 30 years, and the SIV subtype H1N2 has been circulating since it was first isolated in Great Britain in 1994 [2, 3]. In April 2009, a new influenza A virus of subtype H1N1 emerged in the human population in Mexico and the United States. This was a multiple reassortant virus containing genes from North American and Eurasian lineages [4, 5]. The virus spread rapidly across the world by human-to-human transmission. Human-to-pig transmission was first reported in Canada in late April 2009, then in European pig population in early September 2009, and has since been reported in several countries all over the world [6–9]. In October 2009, SIV was reported for the first time in Norway when an integrated pig herd tested positive for pandemic (H1N1) 2009 virus after showing mild clinical signs of respiratory disease [10]. The clinical picture of pandemic (H1N1) 2009 infections in experimentally and naturally infected pigs was described as mild respiratory illness, increased temperature, and decreased appetite [6, 11, 12]. In some infected herds, clinical signs were not detected [13]. Studies have shown that immunological na？ve pigs experimentally infected with pandemic (H1N1) 2009 virus could transmit the virus efficiently to other na？ve pigs [11, 14, 15]. Although pandemic (H1N1) 2009 virus contains gene segment genetically related to other swine influenza virus strains circulating in Europe and North America, it shows antigenetic differences in the major glycoproteins of the virus
References
[1]
K. Van Reeth, I. H. Brown, R. Dürrwald et al., “Seroprevalence of H1N1, H3N2 and H1N2 influenza viruses in pigs in seven European countries in 2002-2003,” Influenza and other Respiratory Viruses, vol. 2, no. 3, pp. 99–105, 2008.
[2]
J. Maldonado, K. Van Reeth, P. Riera et al., “Evidence of the concurrent circulation of H1N2, H1N1 and H3N2 influenza A viruses in densely populated pig areas in Spain,” Veterinary Journal, vol. 172, no. 2, pp. 377–381, 2006.
[3]
I. H. Brown, “The epidemiology and evolution of influenza viruses in pigs,” Veterinary Microbiology, vol. 74, no. 1-2, pp. 29–46, 2000.
[4]
R. J. Garten, C. T. Davis, C. A. Russell et al., “Antigenic and genetic characteristics of swine-origin 2009 A(H1N1) influenza viruses circulating in humans,” Science, vol. 325, no. 5937, pp. 197–201, 2009.
[5]
J. Cohen, “Swine flu outbreak. New details on virus's promiscuous past,” Science, vol. 324, no. 5931, p. 1127, 2009.
[6]
S. E. Forgie, J. Keenliside, C. Wilkinson et al., “Swine outbreak of pandemic influenza A virus on a canadian research farm supports human-to-swine transmission,” Clinical Infectious Diseases, vol. 52, no. 1, pp. 10–18, 2011.
[7]
A. Moreno, T. L. Di, L. Alborali , et al., “First pandemic H1N1 outbreak from a pig farm in Italy,” The Open Virology Journal, vol. 4, pp. 52–56, 2010.
[8]
T. Pasma and T. Joseph, “Pandemic (H1N1) 2009 infection in swine herds, Manitoba, Canada,” Emerging Infectious Diseases, vol. 16, no. 4, pp. 706–708, 2010.
[9]
M. D. Welsh, P. M. Baird, M. P. Guelbenzu-Gonzalo et al., “Initial incursion of pandemic (H1N1) 2009 influenza A virus into European pigs,” Veterinary Record, vol. 166, no. 21, pp. 642–645, 2010.
[10]
M. Hofshagen, B. Gjerset, and C. Er, “Pandemic influenza A(H1N1)v: human to pig transmission in Norway?” Euro Surveillance, vol. 14, no. 45, 2009.
[11]
S. M. Brookes, A. Nú？ez, B. Choudhury et al., “Replication, pathogenesis and transmission of pandemic (H1N1) 2009 virus in non-immune pigs,” PLoS One, vol. 5, no. 2, Article ID e9068, 2010.
[12]
P. K. Holyoake, P. D. Kirkland, R. J. Davis et al., “The first identified case of pandemic H1N1 influenza in pigs in Australia,” Australian Veterinary Journal, vol. 89, no. 11, pp. 427–431, 2011.
[13]
N. Busquets, J. Segalés, L. Córdoba et al., “Experimental infection with H1N1 European swine influenza virus protects pigs from an infection with the 2009 pandemic H1N1 human influenza virus,” Veterinary Research, vol. 41, no. 5, article 74, 2010.
[14]
E. Lange, D. Kalthoff, U. Blohm et al., “Pathogenesis and transmission of the novel swine-origin influenza virus A/H1N1 after experimental infection of pigs,” Journal of General Virology, vol. 90, no. 9, pp. 2119–2123, 2009.
[15]
A. L. Vincent, K. M. Lager, K. S. Faaberg et al., “Experimental inoculation of pigs with pandemic H1N1 2009 virus and HI cross-reactivity with contemporary swine influenza virus antisera,” Influenza and other Respiratory Viruses, vol. 4, no. 2, pp. 53–60, 2010.
[16]
C. S. Kyriakis, C. W. Olsen, S. Carman et al., “Serologic cross-reactivity with pandemic (H1N1) 2009 virus in pigs, Europe,” Emerging Infectious Diseases, vol. 16, no. 1, pp. 96–99, 2010.
[17]
B. Lium, A. Germundsson, C. Er, and P. Hopp, “The surveillance and control programme for specific virus infections in swine herds in Norway,” in Surveillance and control programmes for terrestrial and aquatic animals in Norway, annual report 2010, pp. 1–8, National Veterinary Institute, 2011.
[18]
B. Lium, A. Jorgensen, and M. Gjestvang, “The Norwegian program for eradication of Mycoplasma hyopneumoniae is successfully completed,” in Proceedings of the 21st IPVS Congress, p. 643, 2010.
[19]
Office International des Epizooties, Manual of standards for diagnostic tests and vaccines for terrestrial animals (mammals, birds and bees), vol. 1, 6th edition, 2010.
[20]
World Health Organization, The WHO Collaborating Centre for influenza at CDC Atlanta,United States of America. CDC protocol of realtime RTPCR for influenza A(H1N1), WHO, Atlanta, Ga, USA, 2009, http://www.who.int/csr/resources/publications/swineflu/CDCRealtimeRTPCR_SwineH1Assay-2009_20090430.pdf.
[21]
Robert Koch-Institut, “TagMan real-time PCR zur Detektion von porcinen Influenza A/H1N1-Viren. Empfehlung für den Nachweis der porcinen Influenza A/H1N1-Viren mittels real-time PCR,” 2010, http://www.rki.de/cln_160/nn_200120/DE/Content/InfAZ/I/Influenza/IPV/Schweinegrippe__PCR.html.
[22]
World Health Organization, The WHO Collaborating Centre for influenza at CDC Atlanta, United States of America. Sequencing primers and protocol, WHO, Atlanta, Ga, USA, 2009, http://www.who.int/entity/csr/resources/publications/swineflu/GenomePrimers_20090512.pdf.
[23]
T. A. Hall, “BioEdit: a user-friendly biological sequence alignment editor and analysis program for Windows 95/98/NT,” pp. 95–98, 1999.
[24]
K. Waalen, A. Kilander, S. G. Dudman, G. H. Krogh, T. Aune, and O. Hungnes, “High prevalence of antibodies to the 2009 pandemic influenza A(H1N1) virus in the Norwegian population following a major epidemic and a large vaccination campaign in autumn 2009,” Eurosurveillance, vol. 15, no. 31, 2010.
[25]
R. Tellier, “Aerosol transmission of influenza A virus: a review of new studies,” Journal of the Royal Society Interface, vol. 6, no. 6, pp. S783–S790, 2009.
[26]
I. A. Gardner, P. Willeberg, and J. Mousing, “Empirical and theoretical evidence for herd size as a risk factor for swine diseases,” Animal Health Research Reviews, vol. 3, no. 1, pp. 43–55, 2002.
[27]
K. M. Grebe, J. W. Yewdell, and J. R. Bennink, “Heterosubtypic immunity to influenza A virus: where do we stand?” Microbes and Infection, vol. 10, no. 9, pp. 1024–1029, 2008.
[28]
K. Van Reeth, V. Gregory, A. Hay, and M. Pensaert, “Protection against a European H1N2 swine influenza virus in pigs previously infected with H1N1 and/or H3N2 subtypes,” Vaccine, vol. 21, no. 13-14, pp. 1375–1381, 2003.
[29]
C. S. Kyriakis, I. H. Brown, E. Foni et al., “Virological surveillance and preliminary antigenic characterization of influenza viruses in pigs in five European countries from 2006 to 2008,” Zoonoses and Public Health, vol. 58, no. 2, pp. 93–101, 2011.
[30]
W. A. Howard, S. C. Essen, B. W. Strugnell et al., “Reassortant pandemic (H1N1) 2009 virus in pigs, United Kingdom,” Emerging Infectious Diseases, vol. 17, no. 6, pp. 1049–1052, 2011.
[31]
Y. Bi, G. Fu, J. Chen et al., “Novel swine influenza Virus reassortants in Pigs, China,” Emerging Infectious Diseases, vol. 16, no. 7, pp. 1162–1164, 2010.
[32]
P. Kitikoon, D. Sreta, S. Nuntawan Na Ayudhya et al., “Brief report: molecular characterization of a novel reassorted pandemic H1N1 2009 in Thai pigs,” Virus Genes, vol. 43, no. 1, pp. 1–5, 2011.
[33]
D. Vijaykrishna, L. L. M. Poon, H. C. Zhu et al., “Reassortment of pandemic H1N1/2009 influenza a virus in swine,” Science, vol. 328, no. 5985, p. 1529, 2010.
