Wu Yaotang, Wu Yang, Wang Chenlu, Xiong Ningna, Ji Wenxin, Fu Mei, Zhu Junpeng, Li Zhixin, Lin Jian, Yang Qian
College of Veterinary Medicine, Nanjing Agricultural University, Wei gang 1, Nanjing, Jiangsu, 210095, China.
College of Life Sciences, Nanjing Agricultural University, Wei gang 1, Nanjing, Jiangsu, 210095, China.
Cell Mol Life Sci. 2025 Feb 22;82(1):89. doi: 10.1007/s00018-025-05603-1.
RNA interference (RNAi) and autophagy are two pivotal biological processes that regulate virus replication. This study explored the complex relationship between autophagy and RNAi in controlling influenza virus replication. Initially, we reported that influenza virus (H9N2) infection increases the viral load and the expression of autophagy markers while inhibiting the RNAi pathway. Subsequent studies employing autophagy enhancer and inhibitor treatments confirmed that avian influenza virus (AIV, H9N2) promotes viral replication by enhancing autophagy pathways. Further analysis revealed that ATG7, an autophagy protein, can interact with dicer to affect its antiviral functions. Finally, we discovered that infection with other avian RNA viruses, including infectious bursal disease virus (IBDV) and infectious bronchitis virus (IBV), induced the upregulation of ATG7, which blocked the RNAi pathway to facilitate virus replication. Our findings suggested that virus infection might trigger the upregulation of autophagy and downregulation of the RNAi pathway, revealing a complex interaction between these two biological processes in the defence against viral replication.
RNA干扰（RNAi）和自噬是两个调节病毒复制的关键生物学过程。本研究探讨了自噬与RNAi在控制流感病毒复制过程中的复杂关系。最初，我们报道流感病毒（H9N2）感染会增加病毒载量和自噬标志物的表达，同时抑制RNAi途径。随后使用自噬增强剂和抑制剂处理的研究证实，禽流感病毒（AIV，H9N2）通过增强自噬途径促进病毒复制。进一步分析表明，自噬蛋白ATG7可与Dicer相互作用，影响其抗病毒功能。最后，我们发现感染其他禽RNA病毒，包括传染性法氏囊病病毒（IBDV）和传染性支气管炎病毒（IBV），会诱导ATG7上调，从而阻断RNAi途径以促进病毒复制。我们的研究结果表明，病毒感染可能会引发自噬上调和RNAi途径下调，揭示了这两个生物学过程在抵御病毒复制中的复杂相互作用。
