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块性皮肤病病毒通过动氨酸介导的内细胞和巨细胞细胞分裂进入宿主细胞
Shasha Wang1, Pengyuan Cheng1, Ke Guo1
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.
Veterinary microbiology
|September 22, 2024
概括
型皮肤病病毒 (LSDV) 通过巨型皮细胞分裂 (macropinocytosis) 进入牛细胞,这一过程需要低pH和动氨酸. 这一发现为潜在的治疗开发提供了对LSDV感染机制的见解.
科学领域:
- 兽医病毒学 兽医病毒学
- 细胞生物学 细胞生物学
- 传染性疾病 传染性疾病
背景情况:
- 结节性皮肤病病毒 (LSDV) 在牛群中造成重大经济损失,是需要报告的疾病.
- 细胞进入机制和LSDV的调节分子在很大程度上仍然没有表征.
研究的目的:
- 阐明LSDV进入牛细胞时使用的内细胞通路.
- 确定关键的细胞因素和调节LSDV细胞吸收的条件.
主要方法:
- 使用药理抑制剂阻断马丁-达比牛 (MDBK) 和牛乳腺上皮细胞 (BMEC) 中的特定内细胞通路.
- 评估了抑制剂对LSDV进入和结合细胞的影响.
- 研究了低pH,动,洞穴,克拉,Na+/H+交换器 (NHE) 和酸丁醇3-激酶 (PI3K) 在LSDV吸收中的作用.
主要成果:
- LSDV进入MDBK和BMEC细胞取决于低pH条件和蛋白质动氨酸.
- 洞穴和克拉特林介导的内细胞分裂与LSDV的进入无关.
- LSDV的吸收通过巨型皮诺细胞体发生,依赖于Na+/H+交换器 (NHE),但独立于PI3K.
- 抑制剂影响了LSDV的进入,但没有影响病毒与细胞的结合.
结论:
- 对于细胞进入牛细胞,LSDV利用了宏皮诺细胞形成的途径.
- 这种进入机制的特点是低pH的依赖性和胺的参与,同时独立于PI3K.
- 了解LSDV的进入机制为开发针对疾病的有针对性的治疗干预提供了基础.
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