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GSDMD和GSDME在肠道冠状病毒PDCoV诱导的热和炎症反应中表现出不同的作用
Chenyu Li1,2, Yuting Shi1,2, Chunying Xie1,2
1Key Laboratory of Preventive Veterinary Medicine in Hubei Province, Cooperative Innovation Center for Sustainable Pig Production, Wuhan, China.
Journal of virology
|June 12, 2025
概括
猪三角型冠状病毒 (PDCoV) 触发了细胞灭绝,一种被编程的细胞死亡,GSDME在炎症中发挥了主导作用. PDCoV蛋白酶分裂GSDMD,阻碍其抗病毒功能并促进感染.
科学领域:
- 兽医病毒学 兽医病毒学
- 免疫学 免疫学 免疫学
- 细胞病理学细胞病理学
背景情况:
- 猪三角冠状病毒 (PDCoV) 在猪中引起肠道疾病和炎症.
- 炎症性编程细胞死亡的 Pyroptosis 与病毒病原发生有关.
- 气体皮质D (GSDMD) 和气体皮质E (GSDME) 在PDCoV感染中的特定作用尚不清楚.
研究的目的:
- 为了调查PDCoV感染诱导热的原因.
- 阐明GSDMD和GSDME在PDCoV诱导的热和炎症中的不同作用.
- 确定PDCoV干扰热的机制.
主要方法:
- 猪皮上皮细胞系感染PDCoV.
- 分析PDCoV感染小猪感染的感染细胞和组织中的烧死标记物.
- 通过PDCoV非结构蛋白5 (3C类蛋白酶) 检测GSDMD和GSDME的裂变.
主要成果:
- 感染PDCoV会触发GSDMD和GSDME介导的灭.
- GSDME在PDCoV诱导的热和随后的炎症反应中发挥着主导作用.
- 类似PDCoV 3C的蛋白酶可以切割GSDMD,但不能切割GSDME,从而降低了GSDMD的抗病毒和火性功能.
结论:
- 感染PDCoV诱导热,GSDME是炎症反应的主要媒介.
- PDCoV利用其3C类蛋白酶来切割GSDMD,从而逃避宿主抗病毒防御.
- 了解GSDMD和GSDME的不同作用,可以深入了解PDCoV病原和潜在的治疗点.
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