代谢劫持的多omics解剖:传染性支气管炎病毒通过PPAR-TGF-β交叉连接协调脂质中心的复制
Kun Yan1, Xiuling Wang1, Zongyi Bo1,2
1Jiangsu Co-Innovation Center for the Prevention and Control of Animal Infectious Disease and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China.
Virulence
|January 22, 2026
概括
禽传染性支气管炎病毒 (IBV) 重新编程宿主新陈代谢,重定向葡萄糖和脂质以推动病毒复制. 针对关键的代谢途径和像PPAR-TGF-β这样的信号提供了潜在的抗病毒策略来对抗这种具有经济意义的家禽疾病.
科学领域:
- 病毒学和宿主-病原体相互作用
- 代谢学和脂质学
- 分子生物学和免疫学 分子生物学和免疫学
背景情况:
- 鸟类传染性支气管炎病毒 (IBV),一种马冠状病毒,由于多系统性疾病,在家禽中造成重大经济损失.
- 控制IBV与宿主代谢网络之间的相互作用的复杂分子机制尚未得到充分理解.
- 理解宿主代谢重编程对于开发有效的抗病毒干预措施至关重要.
研究的目的:
- 为了阐明IBV感染在卵管组织中诱导的代谢重编程.
- 为了确定关键的宿主代谢途径和信号网络,IBV.
- 探索基于代谢干预的潜在宿主向抗病毒策略.
主要方法:
- 来自IBV感染的无特定病原体 (SPF) 的卵管组织的综合转录基因,代谢基因和脂质基因分析.
- 对代谢流量,基因表达和脂质积累的分析.
- 针对关键代谢酶和信号通路的抗病毒策略的体外验证.
主要成果:
- 证明了三方代谢重编程:增强酸通路 (PPP) 活性,优先考虑膜生物发生的新型脂质生成,并改变了甘油脂代谢.
- 确定IBV利用Warburg效应和PPP激活,加上抑制的脂肪酸氧化,促进脂质滴生物发生.
- 发现过度生产的脂 (PS),以及由脂酶A2 (PLA2) 调节的脂 (Lyso-PLs) 和eicosanoids (例如,PGE2) 的增加,与PPAR和TGF-β通路激活相关.
结论:
- 感染IBV引发了一个协调的代谢转变,有利于核酸和脂质合成病毒传播.
- 过氧体增殖器激活受体 (PPAR) 和转化生长因子-β (TGF-β) 信号传输之间的关键交谈控制了IBV感染期间的脂质重塑和免疫调节.
- 向宿主代谢节点,特别是乙-CoA碳糖酶 (ACC),葡萄糖-6-酸盐脱酶 (G6PD) 和TGF-β通路,表明了协同的抗病毒潜力.
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