ArticlePoultry science2026
Impact of GAstV-2 infection on intestinal microbiota and renal gene transcriptome in goslings.
Article in Poultry science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Goose astrovirus-2 (GAstV-2) is the major etiological agent responsible for hyperuricemia and visceral gout in goslings, which causes substantial economic losses to the goose-raising industry. However, the complete pathogenic mechanisms underlying GAstV-2-induced hyperuricemia have not been fully elucidated. In this study, 1-day-old healthy Yangzhou goslings were orally inoculated with GAstV-2 to establish a viral infection model. The effects of GAstV-2 infection on growth performance, serum uric acid levels, cecal microbiota structure, and renal gene expression of goslings were systematically investigated. The results showed that GAstV-2 infection caused a cumulative mortality rate of 10%-30% in goslings and significantly impaired growth performance, as reflected by decreased average daily gain and average daily feed intake as well as an increased feed-to-gain ratio (P < 0.05). In addition, GAstV-2 challenge induced severe histopathological damage to the liver and kidney, disordered serum biochemical metabolism, and excessive release of pro-inflammatory cytokines, accompanied by a significant elevation in serum uric acid levels (P < 0.05). The 16S rRNA high‑throughput sequencing results confirmed that GAstV‑2 infection significantly decreased the abundances of uric acid‑degrading beneficial bacteria, including Paenibacillus polymyxa, Oscillospira guilliermondii, and Lactococcus lactis, while markedly increasing the abundance of Clostridium perfringens, which is closely associated with uric acid synthesis. Renal transcriptomic analysis confirmed that key genes involved in purine metabolism, including PRPS, IMPDH1, and NT5E, were significantly upregulated in the kidney tissues of infected goslings, which was closely correlated with the occurrence of hyperuricemia. In conclusion, GAstV-2 infection markedly inhibits growth, triggers hepatic and renal injury, increases serum uric acid and inflammatory levels, and remodels the intestinal microbiota composition and renal transcriptomic profiles in goslings. This study systematically explored the influences of GAstV-2 infection on growth performance, hepatorenal injury, and serum uric acid metabolism in goslings, and preliminarily revealed the potential underlying mechanism of GAstV-2-induced hyperuricemia by separately analyzing intestinal microbiome and renal transcriptome data. These findings provide fundamental data and a theoretical basis for further elucidating the pathogenic mechanism of GAstV-2 and developing targeted prevention and control strategies against gosling gout.
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