Ducks, the reservoir host, are generally permissive to influenza A virus infection without disease symptoms. This natural ecology was upset by the emergence of H5N1 strains, which can kill ducks. To better understand host-virus interactions in the reservoir host, and influenza strain-specific molecular contributions to virulence, we infected White Pekin ducks with three similar H5N1 viruses, with known differences in pathogenicity and replication rate. We quantified viral replication and innate immune gene activation by qPCR, in lung and spleen tissues, isolated on each of the first 3 days of infection. The three viruses replicated well, as measured by accumulation of matrix gene transcript, and viral load declined over time in the spleen. The ducks produced rapid, but temporally limited, IFN and cytokine responses, peaking on the first day post-infection. IFN and proinflammatory cytokine gene induction were greater in response to infection with the more lethal viruses, compared to an attenuated strain. We conclude that a well-regulated IFN response, with the ability to overcome early viral immune inhibition, without hyperinflammation, contributes to the ability of ducks to survive H5N1 influenza replication in their airways, and yet clear systemic infection and limit disease.
Keywords: H5N1; cytokine; duck; inflammation; influenza A; interferon.