2. Academic Validation
  3. Infectious bronchitis virus (IBV) triggers autophagy to enhance viral replication by activating the VPS34 complex

Infectious bronchitis virus (IBV) triggers autophagy to enhance viral replication by activating the VPS34 complex

  • Microb Pathog. 2024 May:190:106638. doi: 10.1016/j.micpath.2024.106638.
Gaojie Song 1,  Cuiling Zhang 2,  Xiaoyang Yu 3,  Jiaqi Li 4,  Qinlei Fan 5,  Fei Liu 5,  Qinghao He 6,  Chao Shang 7,  Xiao Li 8
Affiliations

Affiliations

  • 1 Jiangxi Provincial Key Laboratory of Systems Biomedicine, Jiujiang University, Jiujiang, China.
  • 2 Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, China.
  • 3 Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, China; College of Veterinary Medicine, Jilin University, Changchun, China.
  • 4 Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, China; Shandong Normal University, Jinan, China.
  • 5 China Animal Health and Epidemiology Center, Qingdao, China.
  • 6 Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, China. Electronic address: qhhe@rcees.ac.cn.
  • 7 Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, China. Electronic address: shangchao1290@126.com.
  • 8 Changchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun, China. Electronic address: 949194331@qq.com.
PMID: 38574829 DOI: 10.1016/j.micpath.2024.106638
Abstract

Autophagy plays an important role in the lifecycle of viruses. However, there is currently a lack of systematic research on the relationship between Infectious Bronchitis Virus (IBV) and Autophagy. This study aims to investigate the impact of IBV on Autophagy and the role of Autophagy in viral replication. We observed that IBV Infection increased the expression of microtubule-associated protein 1 LIGHT chain 3, a marker of Autophagy, decreased the expression of sequestosome 1, and led to elevated intracellular LC3 puncta levels. These findings suggest that IBV Infection activates the autophagic process in cells. To investigate the impact of Autophagy on the replication of IBV, we utilized rapamycin as an Autophagy activator and 3-methyladenine as an Autophagy Inhibitor. Our results indicate that IBV promotes viral replication by inducing Autophagy. Further investigation revealed that IBV induces autophagosome formation by inhibiting the mTOR-ULK1 pathway and activating the activity of vacuolar protein sorting 34 (Vps34), autophagy-related gene 14, and the Beclin-1 complex. Vps34 plays a crucial role in this process, as inhibiting Vps34 protein activity enhances cell proliferation after IBV Infection. Additionally, inhibiting Vps34 significantly improves the survival rate of IBV-infected chicks, suppresses IBV replication in the kidney, and alleviates tracheal, lung, and kidney damage caused by IBV Infection. In summary, IBV Infection can induce Autophagy by modulating the mTOR/ULK1 signaling pathway and activating the Vps34 complex, while Autophagy serves to promote virus replication.

Keywords

Autophagy; IBV; VPS34; Viral replication; mTOR/ULK1 signaling pathway.

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