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Impact of route of exposure and challenge dose on the pathogenesis of H7N9 low pathogenicity avian influenza virus in chickens

Erica Spackman, Mary Pantin-Jackwood, David E. Swayne, David L. Suarez, Darrell R. Kapczynski
Virology 2015 v.477 pp. 72-81
Influenza A virus, White Leghorn, chickens, exposure pathways, genetics, human diseases, influenza, intravenous injection, kidneys, morbidity, mortality, pathogenesis, pathogenicity, patients, virus replication, viruses, China
H7N9 influenza A first caused human infections in early 2013 in China. Virus genetics, histories of patient exposures to poultry, and previous experimental studies suggest the source of the virus is a domestic avian species, such as chickens. In order to better understand the ecology of this H7N9 in chickens, we evaluated the infectious dose and pathogenesis of A/Anhui/1/2013 H7N9 in two common breeds of chickens, White Leghorns (table-egg layers) and White Plymouth Rocks (meat chickens). No morbidity or mortality were observed with doses of 10⁶ or 10⁸EID₅₀/bird when administered by the upper-respiratory route, and the mean infectious dose (10⁶ EID₅₀) was higher than expected, suggesting that the virus is poorly adapted to chickens. Virus was shed at higher titers and spread to the kidneys in chickens inoculated by the intravenous route. Challenge experiments with three other human-origin H7N9 viruses showed a similar pattern of virus replication.