Native EBV VCA Glycoprotein 125

Epstein-Barr virus (EBV) was first identified in Burkitt's lymphoma, and has since been found to be present in Hodgkin's lymphoma, T-cell lymphoma, and other tumors. EBV has been classified as a herpesvirus family, and is also known as human herpesvirus 4 (HHV-4), with a core of DNA encapsulated in an icosahedral capsid. A first infection with EBV induces the production of memory B cells, which reside in the memory B cells of healthy individuals via infected B cells, and may be reactivated when the patient is immunosuppressed or under stress. Humans are the only known host of EBV, and it is estimated that 90% of the world's population is infected with EBV. EBV is the most common cause of infectious mononucleosis in adolescents, but it can cause more serious diseases, i.e., malignant tumors such as nasopharyngeal carcinoma and Hodgkin's lymphoma, and EBV has been identified as the first human oncolytic virus. During the latency phase, the genome of EBV has unique characteristics compared to other viruses. EBV gene variants such as EBNA and latent membrane protein 2a (LMP-2A) lead to the differentiation of primary B cells into the lymphoblastoid cell lineage, the EBNA gene enables efficient transcription and ensures that the viral genome persists in replicating cells, and LMP-2A is highly correlated with the development of lymphomas. EBV can be categorized into type 1 and type 2, which have sequence polymorphisms in the EBV nuclear antigen 2 (EBNA2) and EBNA3 genes. Type 2 EBV has a low capacity for lymphocyte transformation, and co-infection with both type 1 and type 2 viruses can occur.

EBV is transmitted primarily through saliva, where the virus infects and replicates in the epithelial cells of the oropharynx and subsequently infects B cells entering the mouth, or sometimes directly in the mouth after phagocytosis by the epithelial cells. The EBV glycoproteins involved in epithelial and B-cell infections differ in different cell types, during B-cell infection, the gp350/220 glycoprotein of EBV binds to the complement receptor CD21 or CD35 on the surface of the B-cell; during epithelial cell infection, the lack of CD21 results in the use of the gH glycoprotein for attachment. After attachment, three EBV glycoproteins (gH, gL, and gp42) are involved in viral entry into the cell. gp42 binds to HLA class II molecules in B cells, and in epithelial cells lacking HLA class II molecules, viral entry is mediated by a gH-gL complex. The replication process of EBV in epithelial and B cells also differs, in epithelial cells gp42 binds to the gH-gL complex and produces viral particles containing the gp42-gH-gL complex, whereas viruses produced in B cells lack gp42 in the gH-gL complex. These differences allow viruses produced in epithelial cells to effectively infect B lymphocytes, while viruses replicating in B cells have a greater ability to infect epithelial cells. This characteristic also allows the virus to switch between the two types, persisting and spreading in the body, potentially contributing to viral immune escape.

Figure 1. EBV viral entry
(Source: Damania B, et al. 2022)

Native Epstein-Barr virus VCA Glycoprotein 125