In recent years, an infection in geese caused by goose astrovirus (GAstV) has repeatedly occurred in coastal areas of China and rapidly spread to inland provinces. The infection is characterized by joint and visceral gout and is fatal. The disease has caused huge economic losses to China’s goose industry. GAstV is a nonenveloped, single‐stranded, positive‐sense RNA virus. As it is a novel virus, there is no specific classification. Here, we review the current understanding of GAstV. The virus structure, isolation, diagnosis and detection, innate immune regulation, and transmission route are discussed. In addition, since GAstV can cause gout in goslings, the possible role of GAstV in gout formation and uric acid metabolism is discussed. We hope that this review will inform researchers to rapidly develop effective methods to prevent and treat this disease.

The innate antiviral immunity of humans serves as their first line of defence against viral and microbial illnesses. The retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) signaling pathway requires the mitochondrial antiviral signaling protein (MAVS) to function properly. ZDHHCs, a family of acyltransferases, regulate diverse biological processes via interactions with numerous mammalian proteins and viral proteins. However, the role of ZDHHCs in antiviral innate immunity against RNA viruses remains largely elusive. Here, we show that ZDHHC3 downregulates the RLR signaling pathway. Ectopic ZDHHC3 expression reduces RIG-IN- and SeV-mediated IFN-β promoter activity, IRF3 nuclear transduction, and transcription of the IFN-β and ISG genes. Furthermore, ectopic expression of ZDHHC3 decreases MAVS stability by promoting proteasomal degradation, which can be reversed by MG132 but not CQ. ZDHHC3 interacts with MAVS and promotes its breakdown by increasing K48-linked ubiquitination rather than K63-linked ubiquitination. ZDHHC3 deletion resulted in increased IFN-β promoter activity and transcription of the IFN-β and ISG genes. ZDHHC3 knockdown promotes subsequent antiviral signaling and reduces viral replication, indicating the role of ZDHHC3 in antiviral innate immunity. In addition, the catalytically inactive mutant ZDHHC3 C157S efficiently reversed the IFN-β promoter activity produced by RIG-IN, which was consistent with the results of 2-BP treatment. Collectively, these data show that ZDHHC3 inhibits the RNA virus-triggered signaling cascade by targeting MAVS and provides new insights into the role of ZDHHC3 in antiviral innate immunity.

Since 2017, an infectious disease characterized by gosling gout and caused by goose astrovirus (GAstV) has affected geese in most major goose-producing regions of China. In this study, a total of 385 geese displaying gout symptoms were sampled from 12 cities in Guangdong Province, China, between 2019 and 2021. RT-PCR analysis revealed that all samples were positive for GAstV (385/385), with GAstV-II being the predominant subtype, accounting for 90.4% (348/385) of the cases. Co-infection with GAstV-I and GAstV-II was detected in 50.4% (194/385) of the samples. Additionally, different GAstV subtypes were successfully isolated using goose embryos, namely GDYJ-21-01 (GAstV-I) and GDZJ-21-01 (GAstV-II). Analysis of viral copy numbers in major pathological tissues following infection of goslings and goose embryos revealed that GDZJ strain exhibited broader tissue tropism than GDYJ strain. Compared to other tissues, GDYJ strain displayed tissue tropism exclusively in the cecal tonsils of goslings and the allantoic fluid of embryos. Structural prediction and alignment using AlphaFold 2.0 identified an α-helix in the S223-A226 region of the GDZJ VP34 protein, while a loop structure was observed in the Q235-Q237 region of the corresponding GDYJ VP34 protein. Furthermore, although the VP27 protein regions of both subtypes contained five β-sheet structures, the overall sequence similarity was relatively low, at 37.1%. This study broadens our understanding of the prevalence differences among GAstV subtypes and provides valuable insights into the development of reagents for preventing these viral infections.

• Cultivated PE promotes M2 macrophage polarization; wild PE inhibits M1 polarization. • RNA-Seq reveals 238 metabolite differences between cultivated and wild PE. • Cultivated PE pomace shows potential as a valuable poultry feed additive.