洪尼病毒结构蛋白VP2通过向IRF3基本调节器来抑制β干扰素的产生
Xinyue Zhu1, Qinting Dong1, Kang Zhang1
1Laboratory of Animal Infectious Diseases and Molecular Immunology, College of Animal Science and Technology, Guangxi University, Nanning, China; Guangxi Zhuang Autonomous Region Engineering Research Center of Veterinary Biologics, Nanning 530004, China; Guangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, Nanning 530004, China; Guangxi Colleges and Universities Key Laboratory of Prevention and Control for Animal Disease, Nanning 530004, China.
Veterinary microbiology
|June 8, 2024
概括
水牛汉尼病毒 (BufHuV) 通过抑制干扰素的产生来逃避牛的免疫反应. 这项研究揭示了BufHuV蛋白质,特别是VP2,抑制了关键的抗病毒信号通路,为病毒病原体提供了洞察力.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 兽医医学 兽医医学 兽医医学
背景情况:
- 水牛亨尼病毒 (BufHuV) 是Picornaviridae家族的成员,在牛中引起肠道疾病,导致亚临床感染和重大经济损失.
- 在全球范围内,BufHuV感染宿主细胞并引起天生的免疫反应的机制在很大程度上仍未被描述.
研究的目的:
- 研究BufHuV与宿主天生的免疫系统之间的相互作用.
- 确定参与调节抗病毒反应的BufHuV蛋白质.
- 阐明BufHuV逃避宿主免疫力的机制.
主要方法:
- 干扰素治疗以评估BufHuV复制.
- 用仙台病毒 (SeV) 或多I:C刺激MDBK和HCT-8细胞以分析先天性免疫信号通路 (IRF3,NF-κB,IFN-β促进体激活).
- 构建和选五个BufHuV蛋白 (VP2,2C,3C,3D) 对它们对IFN-β促进体激活的影响.
- 详细分析VP2对IRF3激活,酸化和核转移的影响.
主要成果:
- 干扰素治疗阻断了BufHuV的复制,而病毒感染损害了宿主抗病毒反应.
- BufHuV感染抑制了干扰素-β (IFN-β) 和干扰素刺激基因 (ISG) 的转录.
- BufHuV蛋白VP2,2C,3C和3D抑制了SeV诱导的IFN-β促进体激活.
- 通过抑制其酸化和核转位,VP2 特别抑制了 IRF3 的激活,并干扰了 MDA5 和 TBK1 的信号传输.
结论:
- BufHuV积极抑制宿主天生的免疫反应,特别是干扰素途径.
- 病毒蛋白VP2通过向IRF3激活,在抑制抗病毒信号传递方面发挥着至关重要的作用.
- 这些发现为BufHuV病原体及其免疫逃避策略提供了新的见解.
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