Velogenic Newcastle disease virus (NDV) strains, which show high mortality in chickens, generally do not cause severe disease in waterfowl such as ducks. To elucidate the difference in the pathogenic mechanisms of NDV between chickens and ducks, a chicken-derived velogenic strain (9a5b) was passaged in domestic ducks five times in their air sacs, followed by 20 times in their brains. Eventually, 9a5b acquired higher intracerebral and intranasal pathogenicity in ducks. The intracerebral pathogenicity index (ICPI) value increased from 1.10 to 1.88. All one-week-old ducks intranasally inoculated with the passaged virus (d5a20b) died by 5 days post-inoculation, whereas 70% of the ducks inoculated with parental 9a5b survived for 8 days. The d5a20b strain replicated in broader systemic tissues in ducks compared with the 9a5b strain. The velogenic profile of 9a5b in chickens was maintained after passaging in ducks. The d5a20b suppressed IFN-β gene expression in duck embryo fibroblasts and replicated more rapidly than 9a5b. A total of 11 amino acid substitutions were found in the P, V, M, F, HN, and L proteins of d5a20b. These results suggest that chicken-derived velogenic NDVs have the potential to become virulent in both chickens and ducks during circulation in domesticated waterfowl populations. RESEARCH HIGHLIGHTSChicken-derived NDV acquired high pathogenicity in ducks with serial passaging.The passaged NDV showed intracerebral and intranasal pathogenicity in ducks.The passaged NDV efficiently replicated in systemic tissues in ducks.Of 11 amino acid substitutions some or all are likely involved in pathogenicity.
Keywords: AOAV-1; Newcastle disease virus; duck; host adaptation; pathogenicity; waterfowl.