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

文献类型： 外文期刊

作者： Zhu, Chunhua 1 ; Zhou, Jiayu 1 ; Chen, Zhen 1 ; Chen, Cuiteng 1 ; Wang, Ziyue 1 ; Yang, Pei 1 ; Fu, Guanghua 1 ; Liu, Xiaodong 2 ; Huang, Yu 1 ; Wan, Chunhe 1 ;

作者机构： 1.Fujian Acad Agr Sci, Inst Anim Husb & Vet Med, Fujian Prov Key Lab Avian Dis Control & Prevent, Fuzhou, Peoples R China

2.Fujian Acad Agr Sci, Inst Biotechnol, Fuzhou, Peoples R China

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 ）

ISSN：

年卷期： 2025 年 13 卷 5 期

页码：

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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