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关酸盐结合蛋白5与病毒葡萄糖蛋白的抗作用是独立于蛋白处理的

Hana Veler¹, Cheng Man Lun¹, Abdul A Waheed¹

¹Virus-Cell Interaction Section, HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, USA.

|August 30, 2024

概括

关酸结合蛋白5 (GBP5) 通过破坏病毒葡萄糖蛋白N相关的糖化和细胞表面表达来阻碍包裹病毒的感染性. 这种宿主天生的免疫反应损害了糖蛋白的贩运,而不是蛋白的裂解,提供了新的抗病毒见解.

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:

关酸结合蛋白 (GBP) 5是一种干扰素诱导蛋白,具有已知的抗病毒特性.
GBP5已涉及对抗包裹病毒,可能是通过干扰宿主的病毒糖蛋白分裂.
病毒包膜糖蛋白对于病毒的进入至关重要,并且是适应性免疫系统的目标.

研究的目的:

研究GBP5对广泛的包裹病毒产生敌对作用的机制.
为了确定GBP5的抗病毒活性是否依赖于抑制病毒葡萄糖蛋白的氨酸介导裂变.
阐明GBP5对病毒葡萄糖蛋白糖化,细胞表面表达和病毒结合的影响.

主要方法:

在产生病毒的细胞中表达5英.
对病毒葡萄糖蛋白N相关的糖化模式的分析.
流细胞计,以评估病毒葡萄糖蛋白的细胞表面表达.
对病毒葡萄糖蛋白融入后代病毒颗粒的量化.
在GBP5-表达细胞中产生的病毒的传染性测试.

主要成果:

GBP5表达损害了病毒的传染性,包括依赖氨酸和独立糖蛋白.
GBP5 破坏了正确的N链蛋白糖化,并减少了病毒糖蛋白融入病毒颗粒.
病毒葡萄糖蛋白 (HIV-1 Env,SARS-CoV S,SARS-CoV-2 S) 的细胞表面表达减少了5英.
抑制furin裂变并不是主要的抗病毒机制;观察到血膜的糖蛋白贩运受损.

结论:

GBP5在很大程度上对抗病毒葡萄糖蛋白的功能,独立于素分裂抑制.
主要机制涉及破坏N-链接的糖化,导致糖蛋白贩运受损,并减少病毒结合.
GBP5代表了一种重要的宿主天生的免疫因子,通过调节糖蛋白处理和呈现,影响病毒的进入.

关键词:

英国5英5英5英艾滋病毒-1 Envv 在 MLV Env 中使用.这是SARS-CoV S.在SARS-CoV-2 S S 这是一个VSV-G.细胞抑制因素的细胞抑制因素.病毒葡萄糖蛋白是病毒的葡萄糖蛋白.

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