病毒对II型干扰素的调节增加了T细胞粘附和病毒传播
Carina Jürgens1, George Ssebyatika1,2, Sarah Beyer1
1Institute of Virology, Hannover Medical School, Hannover 30625, Germany.
bioRxiv : the preprint server for biology
|June 9, 2023
概括
疹病毒 (VZV) 糖蛋白C结合并改变干扰素- (IFN-γ) 的活性. 这种相互作用增强了T细胞粘附和VZV传播,揭示了一个新的病毒免疫逃避策略.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 疹病毒 (Varicella zoster virus,VZV) 在上皮细胞中感染,并通过淋巴细胞 (包括T细胞) 系统传播.
- 干扰素 (IFN) 是一种限制VZV初级感染的细胞因子,但病毒使用机制来逃避这种反应.
- 通过VZV感染从上皮细胞的淋巴细胞而逃避宿主细胞因子反应的精确机制仍然不完全理解.
结论:
- VZV利用糖蛋白C干扰IFN-γ信号,导致通过ICAM1和LFA-1增加T细胞粘附.
- 这种机制有助于VZV从上皮细胞传播到外周血液单核细胞,这是一种新的病毒免疫规避策略.
- 这些发现突出了VZV克服宿主抗病毒防御并促进病毒传播的新途径.
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