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Pathogenesis and transmission of the novel swine-origin influenza virus A/H1N1 after experimental infection of pigs

¹ Institute of Infectology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany
² Institute of Diagnostic Virology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany
³ Institute of Molecular Biology, Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany

Correspondence
Thomas W. Vahlenkamp
thomas.vahlenkamp{at}fli.bund.de

Influenza virus A/H1N1, which is currently causing a pandemic, contains gene segments with ancestors in the 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. Virus excretion in the inoculated pigs was detected in nasal swabs from 1 day post-infection (p.i.) onwards and the pigs developed generally mild symptoms, including fever, sneezing, nasal discharge and diarrhoea. Contact pigs became infected, shed virus and developed clinical symptoms similar to those in the inoculated animals. Plasma samples of all animals remained negative for virus RNA. Nucleoprotein- and haemagglutinin 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 from 3 to 7 days p.i., coinciding with clinical signs. Contact chickens remained uninfected, as judged by the absence of virus excretion, clinical signs and seroconversion.

The GenBank/EMBL/DDBJ accession numbers for the complete genome sequence of novel influenza virus A/H1N1 described in this study are FN401574 [GenBank] –FN401581.

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