EBV infection is primarily transmitted through saliva. Almost all EBV seropositive individuals actively shed the virus in the saliva. The other modes of transmission can be sexual transmission, blood transfusion, solid organ or hematopoietic stem cell transplantation. Epithelial cells and B lymphocytes are the two primary target cells of EBV.
EBV when infects the epithelial cells, replication of virus occurs and new viruses are produced causing lysis of the infected cells. Infection of B cell by EBV can occur either by these newly released viruses from the infected epithelial cells or through direct entry. Infection of B cell is mediated by the viral envelop glycoprotein gP350 with the B cell surface molecule CD21 or also known as complement receptor 2(CR2). During the primary infection in B cells, some of the infected B cells undergo lytic infection and in others the virus remains in the latent form.
In the lytic cells, viral proteins are expressed but are kept under check by the immune system.
Whereas in the latently infected cells, the linear genome of EBV gets circularizes and remains latent as episome in the nucleus of the host cell. The viral protein EBV nuclear antigen 1 (EBNA1) binds to the viral DNA and maintains it in the episomal form in the B cell.
During latency, EBV expresses only a few proteins (six nuclear proteins, two non-coded RNAs; EBER 1 and 2 and three latent membrane proteins; LMP 1, 2A, 2B) which help the virus to escape the recognition from cytotoxic T cells.
In general, EBV infection of the epithelial cells leads to lysis of the cell, whereas infection of the B cells mostly leads to latent infection with transformation of the B cells.
