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.