ArticleTranslational cancer research2020
HLA-DPB1 and Epstein-Barr virus gp42 protein jointly contribute to the development of Hodgkin lymphoma.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- The epidemiology, etiology, and future prophylactic options for cancers in Mainland China.Frontiers in oncology · 2025Review
- Human Leukocyte Antigen-Allelic Variations May Influence the Age at Cancer Diagnosis in Lynch Syndrome.Journal of personalized medicine · 2024Article
- Distributions of the HLA-A, HLA-B, HLA-C, HLA-DRB1, and HLA-DQB1 alleles and haplotype frequencies of 1763 stem cell donors in the Colombian Bone Marrow Registry typed by next-generation sequencing.Frontiers in immunology · 2022Article
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3 authors at 1 institution in 1 country.
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Abstract
backgroundEpstein-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.
methodsThe 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.
resultsThe 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.
conclusionsWe 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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