Pteropus vampyrus TRIM40 是一种通过干扰素刺激的基因,可以对抗RIG-I类受体
Sarah van Tol1, Adam Hage1, Ricardo Rajsbaum1,2,3
1Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Viruses
|November 25, 2023
概括
果蝙蝠通过表达TRIM40,一种免疫抑制蛋白质,耐受尼帕病毒 (NiV) 感染. 这一发现揭示了蝙蝠病毒耐受性的关键机制,与人类致命的NiV结果形成鲜明对比.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 进行比较的基因组学.
背景情况:
- 尼帕病毒 (NiV) 引起人类致命的疾病,但被其天然储存体,旧世界水果蝙蝠 (Pteropodidae) 容忍.
- 三方基因 (TRIM) 蛋白质是E3泛基因酶,对先天性抗病毒免疫至关重要,一些TRIM已知与henipaviruses相互作用.
研究的目的:
- 调查NiV诱导蝙蝠免疫抑制TRIM的假设,促进病毒耐受性.
- 为了比较蝙蝠和人类细胞在NiV感染和对先天免疫刺激的反应期间的TRIM表达和功能.
主要方法:
- 在类动物和人类细胞中评估TRIM40作为干扰素刺激基因 (ISG).
- 在蝙蝠细胞中利用TRIM40敲击来评估其在抗病毒反应中对多种I:C和NiV感染的作用.
- 蝙蝠细胞中的量化NiV标位,有或没有TRIM40敲击.
主要成果:
- TRIM40是类动物细胞中的ISG,但不是人类细胞.
- 蝙蝠TRIM40的 Knockdown 增加了IFNβ,ISG 和多种I:C刺激后的炎症性细胞因子的表达.
- 在16小时内,NiV感染在蝙蝠细胞中调节了TRIM40,而TRIM40倒置降低了NiV标位.
结论:
- 蝙蝠可能已经进化了TRIM40表达,作为控制病毒免疫病原发生和耐受NiV感染的机制.
- TRIM40在促进水果蝙蝠的NiV耐受性方面发挥着重要作用.
- 了解蝙蝠的抗病毒策略为NiV和其他类型的paramyxovirus提供了潜在的治疗点的见解.
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