Abstract
Reduced cellular immune function in patients after liver transplantation easily results in many types of viral infections, such as Epstein-Barr virus. Epstein-Barr virus is a Γ-herpesvirus and is related to many malignant diseases, especially epithelial and lymph tumors. The abnormal interaction of cluster of differentiation 40 with cluster of differentiation 40 ligand and expression of cluster of differentiation 40 ligand are considered closely related to the development of myeloma cells. This study explored the influence and mechanism of Epstein-Barr virus infection on the phenotype and biological behavior of myeloma cells after liver transplantation. Flow cytometry was used to detect coexpression of cluster of differentiation 40 and cluster of differentiation 40 ligand in 10 samples of freshly isolated multiple myeloma cells. Cluster of differentiation 40 and cluster of differentiation 40 ligand were coexpressed in sample Nos. 5, 8, 9, and 10, particularly in sample No. 5. Western blot analysis was used to detect the expression of the Epstein-Barr virus antigens latent membrane protein 1 and Epstein-Barr virus nuclear antigen 2 in the multiple myeloma cell line RPMI 8226 infected with Epstein-Barr virus. The antigen expression indicated that Epstein-Barr virus can infect multiple myeloma virus cells in vitro. Reverse transcription-polymerase chain reaction revealed upregulated expression of cluster of differentiation 40 ligand on the infected RPMI 8226 cells, which may be involved in the anti-apoptosis activity of the infected cells. Confocal microscopy showed that pairs of molecules of cluster of differentiation 40, cluster of differentiation 40 ligand, and latent membrane protein 1 were colocalized on the surface of the infected cells. CXC chemokine receptor 4 was upregulated on the RPMI 8226 cells after Epstein-Barr virus infection. The migratory ability of the infected cells improved in the presence of the chemokine stromal cell-derived factor-1α. Anti-apoptosis and migration are known important biological characteristics of malignant cells. Our results indicate the involvement of Epstein-Barr virus in the origin and development of multiple myeloma. The risk of multiple myeloma increases when Epstein-Barr virus infects B cells in the germinal center, which may result in an anti-apoptosis effect of B cells and an improved ability to migrate from the germinal center to peripheral blood.
Highlights
After liver transplantation, patients are immunosuppressed [1] and become susceptible to all types of infection
After in vitro cultivation of RPMI 8226 cells and the supernatant containing Epstein-Barr virus (EBV), the LMP1 expression in the infected cells was detected by immunofluorescence antibody labeling and flow cytometry (FCM) (Figure 2A)
Ways, Cluster of differentiation 40 (CD40) is similar to LMP1, a viral protein expressed on B cells that have been transformed by EBV
Summary
Patients are immunosuppressed [1] and become susceptible to all types of infection. EBV can infect B cells in vitro and transform them into immortalized lymphoblastoid cell lines. CD40 is expressed in the different stages of B-cell differentiation [6] and in malignant tumor induction by B cells, such as in multiple myeloma (MM). MM is a malignant tumor that originates from plasma cells in the final stage of B-cell differentiation [10]. This study was designed to detect the frequency of CD40 and CD40L coexpression by flow cytometry (FCM) in freshly isolated MM cells from 10 post-liver-transplant patients who developed EBV infection complicated by MM. The aims were to explore the mechanism of the malignant transformation of plasma cells into malignant MM cells and the effects of EBV infection on MM development
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