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Systematic Identification of Host Immune Key Factors Influencing Viral Infection in PBL of ALV-J Infected SPF Chicken.
Viruses ( IF 5.818 ) Pub Date : 2020-01-16 , DOI: 10.3390/v12010114
Manman Dai 1, 2 , Shibing Li 1 , Keyi Shi 1 , Jiayu Liao 1 , Hui Sun 1 , Ming Liao 1, 2
Affiliation  

Although research related to avian leukosis virus subgroup J (ALV-J) has lasted for more than a century, the systematic identification of host immune key factors against ALV-J infection has not been reported. In this study, we establish an infection model in which four-week-old SPF chickens are infected with ALV-J strain CHN06, after which the host immune response is detected. We found that the expression of two antiviral interferon-stimulated genes (ISGs) (Mx1 and IFIT5) were increased in ALV-J infected peripheral blood lymphocytes (PBL). A significant CD8+ T cell response induced by ALV-J appeared as early as seven days post-infection (DPI), and humoral immunity starting from 21 DPI differed greatly in the time scale of induction level. Meanwhile, the ALV-J viremia was significantly decreased before antibody production at 14 DPI, and eliminated at 21 DPI under a very low antibody level. The up-regulated CD8+ T cell in the thymus (14DPI) and PBL (7 DPI and 21 DPI) was detected, indicating that the thymus may provide the output of CD8+ T cell to PBL, which was related to virus clearance. Besides, up-regulated chemokine CXCLi1 at 7 DPI in PBL was observed, which may be related to the migration of the CD8+ T cell from the thymus to PBL. More importantly, the CD8 high+ T cell response of the CD8αβ phenotype may produce granzyme K, NK lysin, or IFN-γ for clearing viruses. These findings provide novel insights and direction for developing effective ALV-J vaccines.

中文翻译:

对ALV-J感染SPF鸡的PBL中影响病毒感染的宿主免疫关键因素的系统鉴定。

尽管与禽白血病病毒J亚组(ALV-J)有关的研究已经持续了一个多世纪,但尚未报道针对ALV-J感染的宿主免疫关键因素的系统鉴定。在这项研究中,我们建立了一个感染模型,其中用ALV-J株CHN06感染四周大的SPF鸡,然后检测到宿主的免疫反应。我们发现在ALV-J感染的外周血淋巴细胞(PBL)中,两个抗病毒干扰素刺激基因(ISG)(Mx1和IFIT5)的表达增加了。由ALV-J诱导的显着CD8 + T细胞反应最早在感染后7天(DPI)出现,并且从21 DPI开始的体液免疫在诱导水平的时间尺度上差异很大。同时,在14 DPI产生抗体之前,ALV-J病毒血症显着降低,并在非常低的抗体水平下以21 DPI消除。检测到胸腺(14DPI)和PBL(7 DPI和21 DPI)中CD8 + T细胞的上调,表明胸腺可能将CD8 + T细胞的输出提供给PBL,这与病毒清除有关。此外,观察到PBL在7 DPI时趋化因子CXCLi1表达上调,这可能与CD8 + T细胞从胸腺向PBL的迁移有关。更重要的是,CD8αβ表型的CD8高+ T细胞应答可能会产生颗粒酶K,NK溶素或IFN-γ,以清除病毒。这些发现为开发有效的ALV-J疫苗提供了新颖的见识和方向。这与清除病毒有关。此外,观察到PBL在7 DPI时趋化因子CXCLi1表达上调,这可能与CD8 + T细胞从胸腺向PBL的迁移有关。更重要的是,CD8αβ表型的CD8高+ T细胞应答可能会产生颗粒酶K,NK溶素或IFN-γ,以清除病毒。这些发现为开发有效的ALV-J疫苗提供了新颖的见识和方向。这与清除病毒有关。此外,观察到PBL在7 DPI时趋化因子CXCLi1表达上调,这可能与CD8 + T细胞从胸腺向PBL的迁移有关。更重要的是,CD8αβ表型的CD8高+ T细胞应答可能会产生颗粒酶K,NK溶素或IFN-γ,以清除病毒。这些发现为开发有效的ALV-J疫苗提供了新颖的见识和方向。
更新日期:2020-01-16
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