人类角质细胞中内源性内素1的下调由简单疹病毒1糖蛋白D排除了超级感染,但不影响NK细胞功能
Joanne Kite1,2, Monica Hill1, Natasha Preston1
1Section of Virology, Department of Microbial Sciences, School of Biosciences, University of Surrey, Guildford GU2 7XH, UK.
The Journal of general virology
|March 12, 2024
概括
简单疹病毒1糖蛋白D (gD) 足以降低nectin1受体的调节,这对于病毒的进入至关重要. 这一过程有助于病毒感染,但不能通过NK细胞进行免疫逃避.
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:
- 病毒通常会降低宿主细胞受体的调节,以促进感染.
- 简单疹病毒1 (HSV1) 糖蛋白D (gD) 与nectin1受体下调有关,但确切的机制尚不清楚.
- 之前的研究表明,传入的病毒 gD 或病毒编码的 ICP0 可能是原因.
研究的目的:
- 为了研究人类角质细胞在HSV1感染期间nectin1下调的机制.
- 确定HSV1糖蛋白D (gD) 在nectin1耗尽中的作用.
- 为了阐明gD介导的nectin1下调对病毒感染和NK细胞免疫逃避的影响.
主要方法:
- 使用 nTERT 人类角质细胞来研究HSV1感染.
- 监测细胞表面上的nectin1,nectin2和转移素受体表达.
- 评估了对病毒蛋白质合成与传入病毒的需求.
- 使用野生型和 ΔgD HSV1 突变物研究了 gD 的作用.
- 评估NK细胞的激活和脱粒.
- 进行超级感染实验以评估病毒阻断.
主要成果:
- 感染HSV1导致nectin1从细胞表面消失,这取决于病毒蛋白质合成,而不是传入的病毒.
- 糖蛋白D (gD) 是必要的,也是足够的,用于nectin1耗尽,独立于ICP0或宿主关闭.
- 野生型HSV1抑制了NK细胞激活,但不仅仅是gD介导的nectin1下调.
- HSV1阻断超级感染的能力依赖于gD,并与nectin1下调调节时间相关.
结论:
- HSV1糖蛋白D (gD) 是关键的病毒蛋白,负责nectin1下调.
- 通过gD介导的nectin1损伤对于有效的HSV1感染至关重要.
- 通过gD对nectin1的降低调节不会导致HSV1对NK细胞的免疫逃避.
- HSV1采用不同的机制来促进病毒的进入和免疫逃避.
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