自噬在清除病毒中发挥重要作用，但许多病毒进化出逃避甚至操纵自噬的能力，相关机制尚未完全清楚。我们前期工作显示，呼吸道合胞病毒（RSV）诱导Balb/c鼠及Hep2细胞自噬增强，自噬促进了RSV复制，且很可能为线粒体自噬。由此设想，RSV通过线粒体自噬调控与线粒体关系密切的其他细胞通路（如凋亡、炎症调控等），营造了有助于病毒复制增殖的良好环境。目前有关线粒体自噬、凋亡与病毒关系的研究非常有限，本项目将通过建立干扰自噬相关蛋白的稳定细胞系，利用自噬基因缺陷鼠等手段，进一步在细胞及动物水平了解自噬对RSV复制、致病的影响；利用共聚焦显微镜等技术，明确RSV诱导了线粒体自噬，探讨线粒体自噬对凋亡的影响，以及凋亡在自噬促RSV复制中的作用和可能机制。该研究将有助于深入理解病毒-宿主相互作用关系，为阐明RSV致病机制、开发新的自噬靶向的抗病毒治疗策略提供科学依据。

Although autophagy plays an important role in eliminating virus, a number of viruses have evolved many strategies to evade or even subvert autophagy for their benefit. The mechanisms are still elusive. Our preliminary work showed that RSV infection could trigger autophagy in Balb/c mice and Hep2 cells, which was beneficial for RSV replication. Our trials also indicated that mitophagy may occur simultaneously. Based on this, the hypothesis is proposed that RSV-induced mitophagy may build a fine cellular microenvironment for virus proliferation by regulating other cellular pathways (such as apoptosis or inflammation regulation). Up till now, there are few studies on the relationship between mitophagy, apoptosis and virus. This study is expected to assess the role of autophagy / mitophagy in RSV proliferation and progression by generating stable autophagy-related gene knockdown cells and knockout mice. Using laser scanning confocal microscope and FACS technology, we aim to explore the effect of RSV infection on mitophagy, the regulation of autophagy / mitophagy on apoptosis, the role of this complex interplay in promoting RSV replication and possible regulatory mechanism. This research contributes to understanding virus-host interaction, enriching our insights into RSV pathogenic mechanism and providing new antiviral options targeting autophagy.