HLA-DPB1 and Epstein-Barr virus gp42 protein jointly contribute to the development of Hodgkin lymphoma.
HLA-DPB1 and Epstein-Barr virus gp42 protein jointly contribute to the development of Hodgkin lymphoma.
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HLA-DPB1和EB病毒gp42蛋白共同促进霍奇金淋巴瘤的发生
DOI：
10.21037/tcr-20-2070
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发表时间：
2020-07
影响因子：
0.9
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Li H;Liu D;Li X
EB病毒（EBV）糖蛋白42（gp 42）通过与B淋巴细胞表面上的人白细胞抗原II（HLA-II）结合进入B淋巴细胞，这一过程涉及其它EBV蛋白（例如，gH/gL和gp 350）。从感染的潜伏状态，病毒可以重新激活并进入快速增殖阶段，这使得EBV能够进一步进入B淋巴细胞和上皮细胞，导致肿瘤发展。EBV是一种与霍奇金淋巴瘤（HL）相关的致瘤病毒，gp 42是EBV感染B淋巴细胞的关键蛋白。然而，gp 42的确切结合模式和能力尚不清楚。通过分子动力学模拟得到了gp 42与HLA-DPB 1结合的模式和形态。通过质粒构建和流式细胞术验证gp 42与HLA-DPB 1的结合效率。HLA-DPB 1的β链与gp 42的α链形成氢键复合物，为亲水性蛋白，分辨率为3.25。当gp 42蛋白浓度为80 µg时，HLA-DPB 1和gp 42之间的结合效率达到峰值（范围，26-31.3%）。我们可以通过降低gp 42的浓度来抑制gp 42与HLA-DPB 1的结合。在随后的实验中，我们将验证是否可以通过破坏氢键和破坏亲水性来阻止gp 42与HLA-DPB 1的结合。这些数据可能对霍奇金淋巴瘤的发展和治疗提供一定的参考价值。
Epstein-Barr virus (EBV) glycoprotein 42 (gp42) enters B lymphocytes by binding to the human leukocyte antigen II (HLA-II) on their surface, in a process involving other EBV proteins (e.g., gH/gL and gp350). From a latent state of infection, the virus may reactivate and enter into a rapid proliferation phase, which enables the further entry of EBV into B lymphocytes and epithelial cells, leading to tumor development. EBV is an oncogenic virus associated with Hodgkin lymphoma (HL), and gp42 is a key protein in EBV infection of B lymphocytes. However, the exact binding pattern and capacity of gp42 are unclear. The patterns and morphologies of gp42 binding to HLA-DPB1 were obtained through molecular dynamics simulation. The binding efficiency of gp42 and HLA-DPB1 was verified by plasmid construction and flow cytometry. The β-chain of HLA-DPB1 and the α-chain of gp42 formed a hydrogen-bonded complex, which was a hydrophilic protein with a resolution of 3.25. The binding efficiency between HLA-DPB1 and gp42 reached its peak (range, 26–31.3%) at a gp42 protein concentration of 80 µg. We can inhibit the binding of gp42 to HLA-DPB1 by reducing the concentration of gp42. In the subsequent experiments, we will verify whether the binding of gp42 to HLA-DPB1 can be prevented by breaking hydrogen bonds and destroying hydrophilicity. These data may provide certain reference value for the development and treatment of Hodgkin’s lymphoma.
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影响因子：
5.4
作者：
Mohl, Britta S.;Chen, Jia;Longnecker, Richard
通讯作者：
Longnecker, Richard
由GP42和GHGL进入糖蛋白介导的Epstein-Barr病毒宿主细胞托管的结构基础。
影响因子：
16.6
作者：
Sathiyamoorthy, Karthik;Hu, Yao Xiong;Mohl, Britta S.;Chen, Jia;Longnecker, Richard;Jardetzky, Theodore S.
通讯作者：
Jardetzky, Theodore S.
影响因子：
16
作者：
Mullen, MM;Haan, KM;Jardetzky, TS
通讯作者：
Jardetzky, TS
影响因子：
9.4
作者：
Maurmann, S;Fricke, L;Jabs, WJ
通讯作者：
Jabs, WJ
影响因子：
5.4
作者：
Lin, Zhen;Swan, Kenneth;Flemington, Erik K.
通讯作者：
Flemington, Erik K.