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Goose Astrovirus Type 2 Causes Intestinal Injury and Disrupts Homeostasis in Goslings
College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Vet. Sci. 2026, 13(1), 15; https://doi.org/10.3390/vetsci13010015
Submission received: 8 December 2025
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Revised: 21 December 2025
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Accepted: 22 December 2025
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Published: 23 December 2025
(This article belongs to the Section Veterinary Microbiology, Parasitology and Immunology)
Simple Summary
Goose astrovirus type 2 (GAstV-2) was first identified in Eastern China in 2018. This virus causes mortality rates of up to 50% in goslings aged 3 to 20 days, resulting in significant economic losses to the goose industry. Infected goslings primarily exhibit urate deposition on the surfaces of visceral organs and in joint cavities, pale and swollen kidneys, and lymphocyte depletion in the spleen. However, as a fecal-oral transmitted pathogen, the interactions between GAstV-2 and digestive system organs, as well as the associated pathological damage, remain poorly understood. In this study, we found that following GAstV-2 infection in goslings, the virus was detectable in all segments of the intestine but not in the esophagus, glandular stomach, or muscular stomach. The highest viral load was observed in the duodenum, where it induced crypt necrosis, shortened villus height, a reduced number of Lgr5+ stem cells, and increased expression of inflammatory cytokines. Conversely, the goslings responded to viral invasion by increasing the number of Paneth cells, enhancing the population of Bim+ stem cells, and upregulating the expression of tight junction proteins. These findings contribute to a better understanding of the pathogenic mechanisms of GAstV-2.
Abstract
Goose astrovirus 2 (GAstV-2) infection leads to visceral gout and swollen kidneys in goslings, causing a 5–50% mortality rate and significant economic losses for goose flocks. While most studies on the virus’s pathological damage have focused on the kidneys, few reports have examined the effects of this fecal-oral pathogen on the digestive system. This study investigated GAstV-2 localization, cellular targets, and its impact on intestinal structure and homeostasis in orally infected goslings. Twenty 1-day-old goslings were randomly assigned to the infected and control groups. Clinical signs, organ lesions, viral distribution, histopathology, and alterations in intestinal cell populations, cytokine expression, and signaling pathways were assessed at 7 days post-infection. GAstV-2 was detected in the duodenum, jejunum, ileum, cecum, and rectum, with the highest viral load in duodenal crypt cells. Infection induced crypt cell necrosis, reduced villus height, decreased villus-to-crypt ratio, and lowered numbers of goblet cells and Lgr5+ intestinal stem cells. In contrast, Paneth cell abundance, Bmi1+ stem cells, and tight junction-related gene expression increased. Inhibition of stem cell differentiation into goblet cells was observed, mediated by modulation of the Notch signaling pathway. Proinflammatory cytokines, including IL-1β, IL-6, IL-8, IL-22, and TNF-α, were markedly upregulated, indicating a strong inflammatory response. These results demonstrate that GAstV-2 preferentially targets duodenal crypt cells, disrupts epithelial renewal, and impairs mucosal barrier function, while triggering compensatory regenerative and immune mechanisms. This study provides new insights into the intestinal pathogenesis of GAstV-2 and identifies potential targets for interventions to mitigate intestinal injury and economic losses in gosling production.
