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

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