Autophagy is a crucial mechanism that regulates cellular homeostasis and eliminates viruses by degrading intracellular substances. However, excessive autophagy can contribute to the development of diseases such as cancer and diabetes. Some viruses exploit the autophagic process to their advantage during replication, thereby harming the host. Autophagy-related genes (ATGs) regulate and mediate various functions of autophagy, and ATG14 is a key subunit of the phosphatidylinositol 3-kinase complex that regulates autophagy. Recent studies have demonstrated that autophagy is involved in nervous necrosis virus (NNV) infection. In this study, we identified ATG14 in the seven-band grouper (Hyporthodus septemfasciatus) and assessed its gene expression in various tissues. ATG14, with a length of approximately 300 bp, was found to interact with other organisms. At 48 h post NNV infection, brain ATG14 expression increased approximately 41-fold relative to uninfected controls. When overexpressed in SSN-1 cells, ATG14 caused an elevation in the expression of NNV RNA1 and 2. Additionally, we identified the expression levels of several signaling molecules involved in NNV infection. Our findings suggest that autophagy, along with several other signaling pathways, plays a role in the response of seven-band groupers to NNV infection. Further research is required to gain a comprehensive understanding of these mechanisms.
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