AKT/mTOR mediated autophagy contributes to the self-replication of canine influenza virus in vivo and in vitro

IF 3.7 2区 生物学 Q2 CELL BIOLOGY Cellular signalling Pub Date : 2025-02-08 DOI:10.1016/j.cellsig.2025.111648
Haobo Qu , Xin Yuan , Kehe Huang , Dandan Liu
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Abstract

The prevalence and spread of canine influenza virus (CIV) pose a threat to the health of dogs and humans. Some studies have shown that autophagy is closely related to virus replication, but the exact relationship between CIV replication and autophagy is still unclear. Therefore, this study investigated the effects of autophagy on CIV replication in vitro and in vivo. The data showed that CIV infection significantly caused respiratory tract damage in mice, upregulated the mRNA/protein levels of CIV replication-related genes and autophagy-related genes. In addition, the activation of autophagy by rapamycin (Rapa) significantly intensified the CIV replication and the respiratory tract damage of mice, while the inhibition of autophagy by 3-Methyladenine (3-MA) significantly alleviated these effects. Data of MDCK cells also demonstrated that CIV promoted self-replication through activating autophagy, and the upregulation of AKT/mTOR by insulin significantly inhibited the CIV replication. In summary, this study showed that CIV could promote self-replication by activating AKT/mTOR mediated autophagy, which provides new ideas for the prevention and treatment of canine influenza.
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AKT/mTOR介导的自噬有助于犬流感病毒在体内和体外的自我复制
犬流感病毒(CIV)的流行和传播对犬类和人类的健康构成了威胁。一些研究表明,自噬与病毒复制密切相关,但CIV复制与自噬之间的确切关系尚不清楚。因此,本研究在体外和体内研究了自噬对CIV复制的影响。数据显示,CIV感染显著导致小鼠呼吸道损伤,CIV复制相关基因和自噬相关基因mRNA/蛋白水平上调。此外,雷帕霉素(Rapa)激活自噬可显著增强小鼠的CIV复制和呼吸道损伤,而3-甲基腺嘌呤(3-MA)抑制自噬可显著减轻这些作用。MDCK细胞的数据也表明,CIV通过激活自噬促进自我复制,胰岛素上调AKT/mTOR可显著抑制CIV复制。综上所述,本研究表明CIV可通过激活AKT/mTOR介导的自噬来促进自我复制,为犬流感的防治提供了新的思路。
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来源期刊
Cellular signalling
Cellular signalling 生物-细胞生物学
CiteScore
8.40
自引率
0.00%
发文量
250
审稿时长
27 days
期刊介绍: Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo. Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms.
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