J Gen Virol
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Published online ahead of print on 10 July 2009 as doi:10.1099/vir.0.014480-0
Journal of General Virology 2009;90:2119.

A more recent version of this article appeared on September 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.014480-0
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Pathogenesis and transmission of the novel swine origin influenza virus A/H1N1 after experimental infection of pigs

Elke Lange, Donata Kalthoff, Ulrike Blohm, Jens P Teifke, Angele Breithaupt, Christina Maresch, Elke Starick, Sasan Fereidouni, Bernd Hoffmann, Thomas C Mettenleiter, Martin Beer and Thomas W Vahlenkamp1

Friedrich-Loeffler-Institut

1 E-mail: thomas.vahlenkamp{at}fli.bund.de

Influenza virus A/H1N1n currently causing a pandemic contains gene segments with ancestors in North American and Eurasian swine lineages. To get insights into virus replication dynamics, clinical symptoms and virus transmission in pigs we infected animals intranasally with influenza virus A/Regensburg/D6/09/H1N1. The inoculated pigs started virus excretion in nasal swabs at 1 day p.i. onwards and developed generally mild symptoms including fever, sneezing, nasal discharge, and diarrhea. Contact pigs became infected, shed virus and developed clinical symptoms similarly to the inoculated animals. Plasma samples of all animals remained negative for viral RNA. NP- and H1-specific antibodies could be detected by ELISA 7 days p.i. CD4+ T-cells became activated immediately after infection and both CD4+ and CD8+ T-cell populations expanded 3 to 7 days p.i. coinciding with clinical signs. Contact chicken remained uninfected as judged by the absence of virus excretion, clinical signs and seroconversion.

Received 19 June 2009; accepted 6 July 2009.


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