菌株特异性差异的reovirus感染的小鼠巨细胞分离与多态性在病毒外囊蛋白 σ3 中
Kay L Fiske1,2, Pamela H Brigleb2,3, Luzmariel Medina Sanchez2,4,5
1Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Journal of virology
|October 21, 2024
概括
哺乳动物的ortoreovirus (reovirus) 菌株T1L通过外部囊蛋白σ3与PirB结合感染巨细胞,可能阻断口服耐受性. 这影响了对重新病毒诱导的炎症和乳病触发因子的理解.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 胃肠病学 胃肠病学
背景情况:
- 哺乳动物的ortoreovirus (reovirus) 菌株T1L和T3D-RV感染了小鼠肠道,但引起了不同的炎症反应.
- 与T3D-RV不同的是,T1L感染与口服免疫耐受性 (LOT) 对饮食抗原的阻塞有关.
- 巨细胞在T1L感染期间透到肠道组织,但它们的作用仍然不清楚.
研究的目的:
- 为了研究巨细胞在REOVIRUS肠道感染中的功能.
- 确定reovirus菌株差异性感染巨细胞的机制.
- 为了确定参与reovirus-macrophage相互作用的病毒和宿主因素.
主要方法:
- 骨髓衍生的巨细胞 (BMDMs) 感染与reovirus菌株和reassortants.
- 对负责特定菌株感染的病毒基因段的分析.
- 关于对联免疫球蛋白类受体B (PirB) 在复原病毒与巨细胞结合中的作用的研究.
主要成果:
- T1L比T3D-RV更有效地感染巨细胞.
- 病毒S4基因段,编码外部囊蛋白σ3,决定了菌株特定的巨细胞感染和结合.
- 雷奥病毒与巨细胞的结合是通过σ3与巨细胞受体PirB之间的相互作用来调节的.
结论:
- 巨细胞的Reovirus T1L感染取决于PirB被 σ3外囊蛋白的参与.
- 这些发现表明,巨细胞在对再病毒的天生的免疫反应中起着作用,可能有助于LOT封锁.
- 了解这种相互作用可能会为乳病 (CeD) 疗法和疫苗开发策略提供信息.
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