Tian Xin, Zhang Rui, Yi Shuang, Chen Yu, Jiang Ying, Zhang Xianwen, Zhang Zhidong, Li Yanmin
Key Laboratory of Veterinary Medicine in Universities of Sichuan Province, College of Animal Husbandry and Veterinary Medicine, Southwest Minzu University, 16 Yihuan Rd., Chengdu 610041, China.
Int J Mol Sci. 2024 Dec 25;26(1):84. doi: 10.3390/ijms26010084.
Canine distemper (CD) is a highly infectious disease of dogs which is caused by canine distemper virus (CDV). Previous studies have demonstrated that CDV infection can induce autophagy in cells. However, the mechanism underlying CDV-induced autophagy remains not fully understood. The CDV non-structural protein V plays a vital role in viral replication and pathogenicity in the host. In this study, we investigated the relationship between the CDV-V protein and autophagy induction and further explored its impact on the viral replication and the mechanism behind this. Our results showed that the V protein induced autophagy via inhibiting the phosphorylation of PI3K, AKT, and mTOR to promote viral replication. The activation or inhibition of PI3K phosphorylation resulted in enhancing or reducing viral replication, respectively. Further studies revealed that the V protein interacted with PI3K to induce cellular autophagy. The present study demonstrated that the CDV-V protein can induce cellular autophagy by inhibiting the PI3K/AKT signaling pathway to enhance viral replication. The results improve the understanding of the molecular mechanism of CDV infection and offer new perspectives for the development of effective treatment and prevention strategies.
犬瘟热（CD）是一种由犬瘟热病毒（CDV）引起的犬类高度传染性疾病。先前的研究表明，CDV感染可诱导细胞自噬。然而，CDV诱导自噬的潜在机制仍未完全阐明。CDV非结构蛋白V在病毒复制和宿主致病性中起着至关重要的作用。在本研究中，我们调查了CDV-V蛋白与自噬诱导之间的关系，并进一步探讨了其对病毒复制的影响及其背后的机制。我们的结果表明，V蛋白通过抑制PI3K、AKT和mTOR的磷酸化来诱导自噬，从而促进病毒复制。PI3K磷酸化的激活或抑制分别导致病毒复制的增强或减少。进一步的研究表明，V蛋白与PI3K相互作用以诱导细胞自噬。本研究表明，CDV-V蛋白可通过抑制PI3K/AKT信号通路诱导细胞自噬，从而增强病毒复制。这些结果增进了对CDV感染分子机制的理解，并为开发有效的治疗和预防策略提供了新的视角。
