2020 ESA Annual Meeting (August 3 - 6)

COS 44 Abstract - Influenza A virus transmission, infection, and immunity in reservoir and spillover hosts

Susan A. Shriner1, Mikaela K. Samsel2 and Jeremy W. Ellis1, (1)National Wildlife Disease Program, USDA National Wildlife Research Center, Fort Collins, CO, (2)USDA National Wildlife Research Center, Fort Collins, CO
Background/Question/Methods

Influenza A viruses (IAVs) are important pathogens at the wildlife/agricultural interface. They are endemic in wild waterfowl, but commonly spillover into poultry, causing economic harm. Understanding infection dynamics and natural routes of transmission in both reservoir and spillover hosts is key to managing epizootics. Because wild waterfowl and commercial poultry do not generally come into contact in many geographic regions across the globe, spillover of IAVs into poultry is likely mediated by bridge hosts or contaminated water. In this study, we assessed IAV transmission from contaminated water and compared infection and immune responses for mallards and chickens as representative reservoir and spillover species. We experimentally exposed groups of chickens and mallards (5 chickens and 5 mallard/group) to one of four IAVs (H1N1, H3N8, H4N6, or H6N2) by providing spiked drinking water. We collected swabs daily across the infection and measured viral RNA excretion using qPCR. We collected blood samples to quantify immune responses using a multi-species ELISA. We also tested a secondary exposure by inoculating birds with the same virus they were originally exposed to 60 days after the initial exposure.

Results/Conclusions

None of the birds became infected with the H1N1 virus after exposure to contaminated water, but all birds in the other virus groups became infected. Generally, mallards shed viral RNA sooner and at higher concentrations compared to chickens. None of the birds in the H1N1 group mounted an immune response after the initial exposure, but all birds in the other groups were positive by day 14 with mallards showing detectable responses sooner than chickens (mean difference = 5.7 days), likely due to delayed onset of infection in the chickens. Both species had detectable antibodies to the H6N2 virus sooner than for the other subtypes (mean 11.0 days for chickens, 5.5 days for mallards). For the secondary exposure, all H1N1 chickens and mallards became infected but birds in the other groups were protected against infection. Overall, chickens were susceptible to infection from each of the wild bird viruses tested and contaminated water was a viable route of transmission. Nonetheless, infection characteristics such as onset of infection post exposure, peak shedding concentration, peak shedding day, and infectious period all varied between species and IAV subtype. Linking these data to mechanistic models is the next step in predicting epidemiologic dynamics. More directly, biosecurity systems targeting the protection of drinking water should be a high priority for farm management.