Metabolic disorders and liver damage in Cherry Valley ducks infected with NGPV are associated with intestinal flora dysbiosis (raw data)

The novel goose parvovirus (NGPV) infection can cause cherry valley ducks to develop short beaks and dwarfism (SBDS), resulting in delayed development and significant economic losses to the poultry industry. The aim of this study is to explore the pathogenesis of NGPV infection in ducklings, identify the key driving factors of infection related growth disorders, and provide scientific basis for the development of effective SBDS prevention and control strategies. Ducks infected with NGPV exhibit a decrease in weight, leg and breast muscle weight, and single muscle cell area. In addition, histopathological analysis confirmed the disruption of intestinal barrier in infected ducklings. NGPV infection also leads to significant changes in the gut microbiota and metabolites, with differential metabolites mainly enriched in metabolic pathways. In addition, liver damage induced by NGPV infection includes significant reduction in liver glycogen storage, upregulation of glucose-6-phosphatase mRNA expression, and downregulation of acetyl CoA carboxylase and fatty acid synthase mRNA expression. Through GO enrichment analysis, differential genes in the liver are centered around the vascular endothelial growth factor receptor (VEGFR) pathway. NGPV infection also leads to significant abnormalities in serum biochemical indicators, which are related to differential bacteria in the ileum. In summary, our research findings indicate that NGPV infection in ducklings can lead to intestinal barrier dysfunction, changes in gut microbiota composition and metabolic characteristics, liver injury, and systemic metabolic imbalance. We propose that these interrelated factors contribute to the etiology of abnormal growth and development in ducks, with gut microbiota dysbiosis being a potential key regulatory factor