基酸盐通过通过PIK3C3介导的自受体通过降解受体阻止了依赖APN的冠状病毒的进入
Yunhang Zhang1,2,3, Na Zhang3, Yue Zhang1
1State Key Laboratory for Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute Chinese Academy of Agricultural Sciences, Lanzhou, China.
Journal of virology
|December 6, 2024
概括
基 (PM) 通过通过PIK3C3介导的自来降解APN受体,有效地抑制像TGEV这样的猪肠道冠状病毒. 这一发现提供了一种新的策略来对抗猪中依赖APN的病毒感染.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 动物科学动物科学
背景情况:
- 猪肠道冠状病毒在猪业中造成重大经济损失,原因是小猪的腹和高死亡率.
- 基 (PM) 已在减少腹和死亡率方面显示出临床疗效,但其作用机制尚不清楚.
研究的目的:
- 阐明基 (PM) 抑制猪肠道冠状病毒的机制.
- 调查PM对氨基酶N (APN) 受体的影响及其在病毒进入中的作用.
主要方法:
- 使用传染性胃肠炎病毒 (TGEV) 和猪呼吸道冠状病毒 (PRCV) 的体外和体外研究.
- 调查PM对APN表达,PIK3C3上调和自的影响.
- 在猪体内实验以确认机制和疗效.
主要成果:
- 通过通过PIK3C3上调调节降低APN受体,PM抑制了TGEV和PRCV感染.
- 通过促进PIK3C3-BECN1-ATG14复合体组合和PIK3C3 Ser249酸化,PM诱导了自.
- 在体内研究证实PM能够触发PIK3C3介导的APN降解,限制TGEV的致病性而没有毒性.
结论:
- 基通过通过PIK3C3介导的自来降解APN受体,阻断TGEV和PRCV内部化.
- 这项研究确定了一种控制依赖APN的冠状病毒的新机制,并提供了预防疾病的潜在策略.
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