简单疹病毒1封面糖蛋白C屏蔽糖蛋白D以保护病毒体免受阻断进入的抗体
McKenna A Hull1, Suzanne M Pritchard1, Anthony V Nicola1
1Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, WA, USA.
bioRxiv : the preprint server for biology
|September 4, 2024
概括
简单疹病毒1糖蛋白C (gC) 保护糖蛋白D (gD) 免受中和抗体的影响,增强病毒的进入. 移除Cg会增加gD抗体的敏感性和病毒中和.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 结构生物学 结构生物学
背景情况:
- 简单疹病毒1 (HSV-1) 的进入依赖于糖蛋白D (gD) 与宿主受体内素-1的相互作用.
- 针对gD的中和抗体对于通过阻断受体结合或gH/gL相互作用来防止病毒进入至关重要.
- HSV采用免疫逃避策略,需要对病毒蛋白的作用进行调查.
研究的目的:
- 研究HSV-1糖蛋白C (gC) 在保护糖蛋白D (gD) 免受抗体介导的中和作用.
- 确定Cg是否影响gD对中和抗体的可访问性,并影响病毒的进入.
主要方法:
- 对野生型HSV-1和缺乏Cg (ΔgC) 的HSV-1对抗-gD抗体敏感性的比较分析.
- 对野生类型与Cg-null病毒中的抗-gD抗体的gD反应性的评估.
- 在中和抗体的存在下,对病毒与 nektin-1 的结合和可溶性 nektin-1 的抑制的评估.
主要成果:
- 与野生型病毒相比,缺乏Cg (ΔgC) 的HSV-1对抗gD单克隆抗体的中和敏感性增加.
- 在HSV-1 ΔgC病毒包裹中的gD显示出对抗gD抗体的增强反应性.
- 通过中和抗gD抗体和可溶性 nektin-1 更容易抑制HSV-1 ΔgC 与 nectin-1 的结合.
结论:
- HSV-1 gC保护了gD的受体结合和gH/gL相互作用的域,使其免受中和抗体的影响.
- 缺少Cg暴露了gD,增加了它对抗体中和的敏感性,并促进了病毒的进入.
- 基基因作为一个关键的免疫逃避因子,通过保护必要的病毒入口糖蛋白.
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