Mechanistic insights into the kidney injury in chickens induced by hypervirulent fowl adenovirus serotype 4

文献类型： 外文期刊

第一作者： Zhu, Chunhua

作者： Zhu, Chunhua;Zhou, Jiayu;Chen, Zhen;Chen, Cuiteng;Wang, Ziyue;Yang, Pei;Fu, Guanghua;Huang, Yu;Wan, Chunhe;Liu, Xiaodong

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关键词： hypervirulent fowl adenovirus serotype 4; autophagosome-like vesicles' delivery; inflammation; kidney injury

期刊名称：MICROBIOLOGY SPECTRUM （ 影响因子：3.8； 五年影响因子：4.1 ）

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年卷期： 2025 年 13 卷 5 期

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收录情况： SCI

摘要： Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and multi-tissue tropism post-infection, resulting in substantial economic losses in the poultry industry. However, the molecular mechanism underlying kidney injury caused by FAdV-4 infection remains unclear. Our results indicated that FAdV-4 infection in chickens induces damage to kidney tissues, characterized by the degeneration and necrosis of kidney epithelial cells, glomerular injury, endoplasmic reticulum stress, and the activation of a robust inflammatory response in the kidney cells. Notably, autophagosome-like vesicles enclosed clusters of viral particles that were transmitted between kidney cells post-infection. There might be a novel mechanism of vesicle-mediated cell-to-cell transmission of hypervirulent FAdV-4 that hijacks autophagosome-like vesicles. We also investigated cellular autophagy in kidney cells in vivo and in vitro during early FAdV-4 infection. The autophagy-related marker proteins LC3B, ATG5, and BECN1 were upregulated post-infection, whereas SQSTM1 was downregulated, indicating that FAdV-4 infection enhances autophagic flux and induces complete autophagy. The viral structural protein Fiber 2 was also observed to colocalize with the autophagy-related marker protein LC3B and the exosome-specific marker protein CD63 in the kidney cells at 24 hpi, suggesting that FAdV-4-induced cellular autophagy promotes viral replication in kidney cells and that autophagosome-like vesicles are involved in early FAdV-4 replication in vivo in chickens. Our results offer novel insights into the pathogenesis of hypervirulent FAdV-4 from the perspective of kidney injury post-infection.

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