鸭甲型肝炎病毒的VP3蛋白介导宿主细胞的吸附和凋亡。,Scientific Reports

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鸭甲型肝炎病毒的VP3蛋白介导宿主细胞的吸附和凋亡。
Scientific Reports ( IF 3.8 ) Pub Date : 2019-11-14 , DOI: 10.1038/s41598-019-53285-0
Yalan Lai _{1,

2,

3} , Ni Zeng _{1,

2,

3} , Mingshu Wang _{1,

2,

3} , Anchun Cheng _{1,

2,

3} , Qiao Yang _{1,

2,

3} , Ying Wu _{1,

2,

3} , Renyong Jia _{1,

2,

3} , Dekang Zhu _{2,

3} , XinXin Zhao _{1,

2,

3} , Shun Chen _{1,

2,

3} , Mafeng Liu _{1,

2,

3} , Shaqiu Zhang _{1,

2,

3} , Yin Wang ₂ , Zhiwen Xu ₂ , Zhengli Chen ₂ , Ling Zhu ₂ , Qihui Luo ₂ , Yunya Liu _{1,

2,

3} , Yanling Yu _{1,

2,

3} , Ling Zhang _{1,

2,

3} , Juan Huang _{1,

2,

3} , Bin Tian _{1,

3} , Leichang Pan _{1,

3} , Mujeeb Ur Rehman _{1,

3} , Xiaoyue Chen _{2,

3}

Affiliation

鸭甲型肝炎病毒（DHAV）引起传染病，主要影响1-4周龄的雏鸭，给鸭业造成相当大的损失。尽管近年来对DHAV进行了许多研究，但对于DHAV-1对宿主感染和发病机理的影响仍然未知。本研究调查了DHAV-1结构蛋白VP3对DHAV-1病毒吸附和凋亡的影响，以探讨VP3在病毒生命周期中的作用。通过qRT-PCR分析了DHAV-1 VP3和一种针对该蛋白的抗体对病毒体吸附的影响。结果表明，兔抗VP3 IgG治疗组的病毒拷贝数显着低于阴性对照组，但高于兔抗DHAV-1 IgG治疗组。该结果表明VP3介导了DHAV-1病毒的吸附，但它不是唯一参与此过程的蛋白质。此外，将真核重组质粒pCAGGS / VP3转染到鸭胚成纤维细胞（DEFs）中，并通过DAPI染色，TUNEL分析和流式细胞仪确定其凋亡率。DAPI染色显示核碎裂和核边缘移动。TUNEL分析结果显示黄色核，流式细胞仪显示凋亡率显着增加。此外，qRT-PCR显示凋亡的caspase-3，-8和-9的转录水平增加，其中caspase-3的增加最大，其次是caspase-9和caspase-8。酶活性分析证实了这些结果。此外，VP3蛋白降低了线粒体膜电位，线粒体凋亡途径中凋亡因子Bak，Cyt c和Apaf-1的转录水平明显上调。这些数据表明VP3在DEF中的表达诱导凋亡，并可能主要通过线粒体介导的内在途径激活caspase-3诱导的凋亡。这些发现为阐明DHAV-1感染和发病机理提供了科学数据。

"点击查看英文标题和摘要"

The VP3 protein of duck hepatitis A virus mediates host cell adsorption and apoptosis.

Duck hepatitis A virus (DHAV) causes an infectious disease that mainly affects 1- to 4-week-old ducklings, resulting in considerable loss to the duck industry. Although there have been many studies on DHAV in recent years, the effects on host infection and pathogenesis of DHAV-1 remain largely unknown. This study investigated the effects of the DHAV-1 structural protein VP3 on DHAV-1 virus adsorption and apoptosis to explore the role of VP3 in the viral life cycle. The effects of DHAV-1 VP3 and an antibody against the protein on virion adsorption was analyzed by qRT-PCR. The results showed that the virus copy number for the rabbit anti-VP3 IgG-treated group was significantly lower than that for the negative control group but higher than that for the rabbit anti-DHAV-1 IgG-treated group. This result indicates that VP3 mediates DHAV-1 virus adsorption but that it is not the only protein that involved in this process. In addition, a eukaryotic recombinant plasmid, pCAGGS/VP3, was transfected into duck embryo fibroblasts (DEFs), and the apoptotic rate was determined by DAPI staining, the TUNEL assay and flow cytometry. DAPI staining showed nucleus fragmentation and nuclear edge shifting. TUNEL assay results revealed yellow nuclei, and flow cytometry indicated a significant increase in the apoptotic rate. In addition, qRT-PCR revealed increased in the transcriptional levels of the apoptotic caspase-3, -8 and -9, with the largest increase for caspase-3, followed by caspase-9 and caspase-8. Enzyme activity analysis confirmed these results. Furthermore, the VP3 protein decreased the mitochondrial membrane potential, and the transcriptional levels of the proapoptotic factors Bak, Cyt c and Apaf-1 in the mitochondrial apoptotic pathway were significantly upregulated. These data suggest that expression of VP3 in DEFs induces apoptosis and may primarily activate caspase-3-induced apoptosis through mitochondrion-mediated intrinsic pathways. The findings provide scientific data to clarify DHAV-1 infection and pathogenesis.

更新日期：2019-11-14

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